Method for relieving pain and regenerating intervertebral disc

ABSTRACT

Disc degeneration and chronic back pain are caused by a transport hindrance of oxygen, nutrients and pH buffer from capillaries in endplates into mid-layer of the intervertebral disc. A fluid absorbing conduit is inserted into the intervertebral disc, drawing and delivering the oxygen, nutrients and pH buffer in fluid of body circulation from capillaries at endplates into the mid-layer of the disc. The disc undergoes thousands of relaxation and compression cycles each day from daily activity of the patient. During relaxation phase, the fluid of body circulation containing oxygen, nutrients, and pH buffer is infused into the fluid absorbing conduit. During compression phase, the oxygen, nutrients, and pH buffer in the fluid absorbing conduit is dispersed into the mid-layer of the disc. The pH buffer, bicarbonate, neutralizes the lactic acid to relieve the discogenic pain. Oxygen inhibits hypoxic inflammation and production of lactic acid to further reduce the discogenic pain. Nutrients nourish the disc cells to rebuild or regenerate the disc matrix. 
     Therapeutic agents can be added into the fluid absorbing conduit or injected into the disc implanted with the fluid absorbing conduit to expedite pain relief and disc regeneration. The therapeutic agents can be pH buffering agent, antibiotic, anti-inflammatory drug, anesthetic, antacid, nutrient, sulfate, anti-depressant, calcium channel blocker, growth factor, cells or other.

CROSS-REFERENCES TO OTHER APPLICATIONS

This application is a continuation-in-part of U.S. patent application Ser. No. 14/756,016, filed on Jul. 21, 2015, which is a continuation-in-part of U.S. application Ser. No. 13/261,607, now U.S. Pat. No. 9,138,254 of national stage application of PCT/US2012/000,158 filed on Mar. 23, 2012, which claims U.S. Provisional 61/572,820 filed on Jul. 21, 2011, U.S. Provisional 61/465,804 filed on Mar. 23, 2011 and U.S. Provisional 61/518,489 filed on May 7, 2011.

FIELD OF INVENTION

This invention relates to methods for relieving back pain and regenerating the intervertebral disc. BACKGROUND

Chronic back pain is an epidemic. Nerve impingement is not seen by CT or MRI in about 85% of back pain patients [Deyo R A, Weinstein J N: Low back pain, N Eng J Med, 344(5) February 363-370, 2001. Boswell M V, et. al.: Interventional Techniques: Evidence-based practice guidelines in the management of chronic spinal pain, Pain Physician, 10:7-111, ISSN 1533-3159, 2007]. In fact, lumbar disc prolapse, protrusion, or extrusion accounts for less than 5% of all low back problems, but are the most common causes of nerve root pain and surgical interventions (Manchikanti L, Derby R, Benyamin R , Helm S, Hirsch J : A systematic review of mechanical lumbar disc decompression with nucleoplasty, Pain Physician; 12:561-572 ISSN 1533-3159, 2009). The cause of chronic back pain in most patients has been puzzling to both physicians and patients. Disc contains no blood vessels. Oxygen, nutrients and pH buffer in fluid of body circulation are diffused from capillaries at endplates into the thick and avascular disc. However, calcified layers begin to fortify the cartilaginous endplates as early as age 16, blocking capillaries and reducing diffusion depths of oxygen, nutrients and pH buffer into the disc. Shallow diffusion zones of oxygen, nutrients and neutral pH do not extend into mid-layer of the disc. Hypoxia triggers formation of lactic acid and inflammation in mid-layer of the disc, resulting in acidic pH 5.5-6.5. Starvation triggers enzymatic degradation of proteoglycans in disc matrix to feed cells and form cavities and fissure in the mid-layer. Lactic acid and inflammatory cytokines leak from fissure to inflame outer annulus, causing chronic discogenic pain. Enzymatic degradation of disc matrix flattens the disc, shifting the compressive load from the thinning disc to facet joints, causing facet strain and pain. Both lactic acid burn and strain of the facet joints are not visible under CT or MRI.

Urinary incontinence is common among women after multiple pregnancies. Weight of the baby partially rests on the bladder, flattening and widening the bladder neck and urethral lumen. The sphincteric action of the urethral smooth muscle cannot contract far enough to close the widened lumen for coaptation of urethral mucosa, resulting in urinary incontinence.

SUMMARY OF INVENTION

Disc degeneration and chronic back pain are caused by a transport hindrance of oxygen, nutrients and pH buffer from capillaries in endplates into mid-layer of the intervertebral disc. A fluid absorbing conduit is inserted into the intervertebral disc, drawing and delivering the oxygen, nutrients and pH buffer in fluid of body circulation from capillaries at endplates into the mid-layer of the disc. The disc undergoes thousands of relaxation and compression cycles each day from daily activity of the patient. During relaxation phase, the fluid of body circulation containing oxygen, nutrients, and pH buffer is infused into the fluid absorbing conduit. During compression phase, the oxygen, nutrients, and pH buffer in the fluid absorbing conduit is dispersed into the mid-layer of the disc. The pH buffer, bicarbonate, neutralizes the lactic acid to relieve the discogenic pain. Oxygen inhibits hypoxic inflammation and production of lactic acid to further reduce the discogenic pain. Nutrients nourish the disc cells to rebuild or regenerate the disc matrix.

Therapeutic agents can be added into the fluid absorbing conduit or injected into the disc implanted with the fluid absorbing conduit to expedite pain relief and disc regeneration. The therapeutic agents can be pH buffering agent, antibiotic, anti-inflammatory drug, anesthetic, antacid, nutrient, sulfate, anti-depressant, calcium channel blocker, growth factor, cells or other.

REFERENCE NUMBERS

-   100 Intervertebral disc -   100A L5-S1 disc -   100B L4-5 disc -   100C L3-4 disc -   101 Fluid-absorbing conduit needle or filament needle -   102 Spinal needle -   103 Guide wire or tube -   104 Strand in filament -   105 Endplate -   106A Superior diffusion zone -   106B Inferior diffusion zone -   107 Capillaries -   108 Calcified layers -   109 Vascular buds in endplates -   110 Window of cannula -   111 Filament gripper of filament needle -   112 Extension bar -   113 Indentation between snagging points -   114 Annular delamination -   115 Epiphysis -   116 Lumen of dilator -   118 Sensory nerve -   119 Epidural space -   120 Indentation between grippers -   121 Fissure -   123 Spinal cord -   124 Pores of sponge filament -   126 Filament, fluid absorbing conduit, sponge, gel, disc shunt, or     scaffold -   126A U-section or distal portion of filament -   126B Second proximal portion of filament -   126C First proximal portion of filament -   127 Cover or wrapper of filament -   128 Nucleus pulposus -   129 Facet joint -   130 Filament needle handle -   131 Nutrients, oxygen, pH buffer, cells or therapeutic agent -   132 Cannula handle -   133 Transverse process -   134 Spinous process -   135 Lamina -   140 Ilium or iliac crest -   142 Superior articular process -   143 Inferior articular process -   152 Bobbin -   159 Vertebral body -   160 Biosynthetic product or molecule -   162 Lactic acid -   163 Contrast agent -   184 Hole or void in tissue -   193 Muscle -   194 Spinal nerve root -   195 Posterior longitudinal ligament -   220 Dilator -   230 Cannula -   231 Snagging point, distal edge or rim of cannula -   268 Lumen of cannula -   269 Lumen of filament needle -   276 Syringe -   277 Cell -   278 Pedicle -   378 Annulus or annular layer -   460 Thin spinal needle -   462 Anchor or toggle -   463 Knot -   492 Funnel into lumen of cannula -   493 Marker on filament needle -   494 Flexible holder of the latch -   495 Latch -   496 Slope or slanted surface of latch -   497 Holder of bobbin -   498 Distal protrusion of cannula handle -   499 Proximal protrusion of cannula handle -   500 Distal protrusion of filament needle handle -   501 Proximal protrusion of filament needle handle -   502 Friction ridges of needle handle -   504 Kambin's Triangle (safe entry into disc) -   505 Skin -   516 Urethra -   517 Urethral lumen -   518 Bladder -   519 Bladder neck -   520 Vagina -   521 Pubis -   522 Uterus -   523 Rectum -   524 Posterior wall of urethra -   525 Forceps -   526 Filament advancer -   527 Stem of filament advancer -   528 Barbs or thread of filament advancer -   529 Cone head of dilator -   530 Removable luer lock or dilator handle -   531 Luer lock for syringe -   532 Urethral smooth muscle -   533 Urethral lumen mucosa

DESCRIPTION OF THE DRAWINGS

FIG. 1 shows capillaries 107 in vertebral bodies 159 providing oxygen, nutrients and pH buffer for the avascular intervertebral disc 100 through diffusion.

FIG. 2 shows diffusion of nutrients/oxygen/pH buffer 131 from capillaries 107 in endplates to feed and maintain cells within the disc 100.

FIG. 3 shows a graph of distance into disc from endplate versus oxygen concentration.

FIG. 4 shows anaerobic production of lactic acid 162 in the mid layer of the disc 100, leaking and burning sensory nerve 118 and spinal nerve 194.

FIG. 5 shows leakage of lactic acid 162, burning or irritating the spinal nerve 194.

FIG. 6 shows calcified layers 108 at the endplates 105, blocking diffusion of nutrient/oxygen/pH buffer 131 from capillaries 107, forming and leaking lactic acid 162 to nerve 118.

FIG. 7 shows vacuoles 184 in the disc 100 from degradation of proteoglycans to release sugars for maintaining survival of disc cells.

FIG. 8 shows load transfer from the flattened disc 100 to facet joint 129 causing facet pain.

FIG. 9 depicts swaying of a vertebral body 159 above a disc 100 with low-swelling pressure.

FIG. 10 depicts spinal instability from the low-pressure disc 100, straining and wearing down the facet joints 129.

FIG. 11 shows insertion of a spinal needle 102 toward the surface of the degenerated disc 100 to prepare for diagnostic discography.

FIG. 12 shows a fluoroscopic anterior-posterior view of the needle 102, about half way past pedicles 278, entering into the disc 100.

FIG. 13 shows a fluoroscopic lateral view of the needle 102 entering into the disc 100 space, but not into the epidural space 119.

FIG. 14 shows a small spinal needle 460 housed within the spinal needle 102, puncturing into the nucleus pulposus 128 of the degenerated disc 100.

FIG. 15 depicts pain diagnostic discography by flushing lactic acid 162 with contrast agent 163 from disc 100 to sensory nerve 118 to provoke and confirm the excruciating pain.

FIG. 16 shows sliding of spinal needle 102 over small spinal needle 460 into nucleus 128.

FIG. 17 shows replacing the small spinal needle 460 with a guide wire 103.

FIG. 18 shows replacing the spinal needle 102 with a cone head 529 dilator 220.

FIG. 19 shows snagging points 231 at the distal end of a cannula 230.

FIG. 20 shows insertion of the cannula 230 sliding over the dilator 220.

FIG. 21 shows a filament needle 101 or fluid-absorbing-conduit needle 101 with at least one filament gripper 111.

FIG. 22 shows a U-shaped filament 126 or fluid absorbing conduit 126 with the U-portion or distal portion 126A extended from the filament needle 101.

FIG. 23 shows insertion of the filament needle 101 with the filament 126 or fluid absorbing conduit 126 into the cannula 230.

FIG. 24 shows the dilator 220 in FIG. 20 is replaced by the needle 101 with the filament 126 or fluid absorbing conduit 126.

FIG. 25 shows the snagging point 231 of the cannula 230 snags the filament strand 126B during partial withdrawal of the needle 101 to deposit a section of filament 126B, 126C in the cannula 230 between distal ends of the cannula 230 and needle 101.

FIG. 26 shows handle 132 of cannula, handle 130 of filament needle 101 and a spool of filament 126 on a bobbin 152 for feeding into the lumen 269 of the filament needle 101 during withdrawal of the needle 101.

FIG. 27 shows re-advancement of the filament needle 101 from FIG. 25, pushing the deposited filament 126B, 126C out of the cannula 230.

FIG. 28 shows filament 126 in nucleus 128 by re-advancing the needle 101.

FIG. 29 shows gripping of the filament 126 by the gripper 111 of the rotating needle 101.

FIG. 30 shows the needle 101 driving the filament 126 to spiral and burrow into tissue, void 184 or fissure 121.

FIG. 31 shows pushing of the needle 101 to pack and burrow the spiraled filament 126 into tissue, void 184 or fissure 121.

FIG. 32 shows snagging of the filament 126 by the snagging point 231 during withdrawal of the filament needle 101 to deposit additional filament 126B, 126C between distal ends of cannula 230 and needle 101.

FIG. 33 shows another re-advancement of the filament needle 101, pushing the additional deposited filament 126B, 126C out of the cannula 230 into tissue.

FIG. 34 shows the needle 101 driving the filament 126 to form another spiral, burrowing into tissue with previously spiraled filament 126.

FIG. 35 shows repeated steps of withdrawal, re-advancement, rotation and pushing of filament needle 101 to form multiple spiraled filaments 126 to bulk, fill or fortify tissue.

FIG. 36 shows withdrawal of the cannula 230 and needle 101 after packing the nucleus 128 of degenerated disc 100 with spirals of filaments 126.

FIG. 37 shows cutting of the filament 126 near the skin 505.

FIG. 38 shows tucking of the filament 126 beneath skin 505 with a long-thin forceps 525.

FIG. 39 shows fluid flowing through the filament 126 from low osmotic pressure in muscle 193 to high osmotic pressure in desiccated disc 100.

FIG. 40 shows a longitudinal view of a disc 100 filled with spiraled filament 126, wicking fluid from muscle 193, superior 106A and inferior 106B diffusion zones into mid layer of disc 100.

FIG. 41 shows thickening of the filament-packed disc 100 to reduce facet loading and pain by lifting the inferior articular process 143 of the facet joint 129.

FIG. 42 shows production of new molecules 160 or disc matrix 160 by cells 277, using the nutrients/oxygen/pH buffer 131 transported through the filament 126 or fluid absorbing conduit 126.

FIG. 43 shows intradiscal injection of nutrients/oxygen/pH buffer 131 and/or cells 277 to facilitate back pain relief and/or disc 100 regeneration.

FIG. 44 shows that the filament 126 or fluid absorbing conduit 126 is totally implanted in the disc 100 by partially withdrawing the cannula 230 for creating head space to implant remaining filament 126 in the filament needle 101.

FIG. 45 shows the filament 126 or fluid absorbing conduit 126 within the disc 100, without extending to outside of the disc 100.

FIG. 46 shows injection of a therapeutic agent 131 or 277 through the cannula 230 into the disc 100.

FIG. 47 shows shielding of L5-S1 disc 100A and L4-5 disc 100B by the iliac crest 140, blocking entry of the straight spinal needle 102 of FIGS. 11 and 14.

FIG. 48 shows iliac crest blocking of the lower lumbar disc 100, preventing entry of spinal needle 102 into the nucleus of the disc 100.

FIG. 49 shows an elastically curved cannula 230 directing a flexible filament needle 101 into the center of the disc 100.

FIG. 50 shows normal position of a bladder neck 519 of a woman with urinary control.

FIG. 51 shows funneling or widening of a bladder neck 519 leading to urinary incontinence.

FIG. 52 shows a small needle 460 within a cone-headed 529 dilator 220 fastened by a removable luer lock 530.

FIG. 53 shows insertion of cannula 230 and needle 101 to implant a spiraled filament 126 in smooth muscle 532 of the bladder neck 519 under cystoscopic or ultrasound guidance.

FIG. 54 shows a cross-sectional view of a widened urethral lumen 517 and initial spiral of the filament 126 within the smooth muscle 532 of the urethra 516.

FIG. 55 shows narrowing of the urethral lumen 517 by bulking the urethral smooth muscle 532 with spirals of filament 126 to allow coaptation of urethral mucosa 533.

FIG. 56 shows two bulking locations of spiraled filaments 126 to close the urethral lumen 533 and relieve urinary stress incontinence.

FIG. 57 shows bulking of the urethral smooth muscle 532 with spiraled filament 126, narrowing the urethral lumen 517 at the bladder neck 519 to regain sphincteric control.

FIG. 58 shows a knot 463 to prevent retraction of the distal end of the filament 126A in the needle 101, and to facilitate filament 126 snagging by the snagging points 231 of cannula 230.

FIG. 59 shows the filament 126C in the needle 101, filament 126B outside the needle 101;

and the filament 126A is the distal portion between filament 126C and filament 126B.

FIG. 60 shows a linear or single stranded filament 126 tied with a knot 463 extending from the needle 101.

FIG. 61 shows an anchor, knob or toggle 462 on a linear filament 126 extending from the needle 101 to facilitate filament 126 snagging by the cannula 230.

FIG. 62 shows a cross bar 111 as a filament gripper 111.

FIG. 63 shows the filament 126 looping over the cross bar 111 for filament 126 spiraling.

FIG. 64 shows a cross plane 111 as a filament gripper 111, dividing the cylindrical lumen 269 into semi-cylinders 269 for housing the filament strand 126C and filament strand 126B.

FIG. 65 shows an extended cross bar 111 as a filament gripper 111 connecting to extension bars 112. The extended cross bar 111 can also be an extended cross plane within the lumen 269.

FIG. 66 shows the filament 126 looping over the extended cross bar 111 or extended cross plane 111 for spiraling and pushing of the filament 126.

FIG. 67 shows cross stubs 111 as a filament gripper 111 for spiraling and pushing of the filament 126.

FIG. 68 shows longitudinal cross stubs 111 along the lumen 269 of the needle 101 for spiraling and pushing of the filament 126.

FIG. 69 shows a filament advancer 526 with resiliently collapsible barbs 528, moving in cyclical distal-proximal motion to advance or propel the filament 126 out of the needle 101.

FIG. 70 shows open (dash line) and closed (solid line) positions of the resiliently collapsible barb 528.

FIG. 71 shows an axial or vertical view of the filament advancer 526 with resiliently collapsible barbs 528 approximately 120 degrees apart.

FIG. 72 shows an axial or vertical view of the filament advancer 526 with resiliently collapsible barbs 528 approximately 90 degrees apart.

FIG. 73 shows a rotational auger 526 as a filament advancer 526 to convey or propel the filament 126 out the needle 101.

FIG. 74 shows a cross section of a needle 101 with a lumen 269 configuration to accommodate the filament advancer 526 and filament 126.

FIG. 75 shows a cannula 230 with multiple snagging points 231.

FIG. 76 shows a cannula 230 with a window 110 open to a snagging point 231.

FIG. 77 shows snagging points 231 of a cannula 230 with inward bending or curvatures.

FIG. 78 shows curvatures of snagging points 231 of another cannula 230.

FIG. 79 shows inward bending or curving walls or gates 231 as snagging points 231 at the distal end of the cannula 230.

FIG. 80 shows a cross-sectional view of the inward bending gates 231 of the cannula 230.

FIG. 81 shows braided strands 104 forming the filament 126.

FIG. 82 shows woven strands 104 forming the filament 126.

FIG. 83 shows knitted strands 104 forming the filament 126.

FIG. 84 depicts a slanted cut of the filament 126, showing the slanted orientations of strands 104 relative to length-wise of the filament 126.

FIG. 85 shows a cross-section of the filament 126 made with parallel strands 104 wrapped, encircled, covered or enveloped by a sheath or cover 127.

FIG. 86 shows a cross-section of the filament 126 made with parallel tubes 104 wrapped, encircled, covered or enveloped by a sheath or cover 127.

FIG. 87 shows a cross-section of the filament 126 made with sponge or foam with pores 124.

FIG. 88 shows a cross-section of a solid filament 126, similar to a mono-filament suture.

FIG. 89 shows a fluid absorbing conduit 126 or filament 126 in disc 100, absorbing nutrients/oxygen/pH buffer 131 from superior diffusion zone 106A and/or inferior diffusion zone 106B of capillaries 107.

FIG. 90 shows a compression phase of the intervertebral disc 100, dispersing the nutrients/oxygen/pH buffer 131 from the fluid absorbing conduit 126 to the mid-layer of the disc 100.

FIG. 91 shows a relaxation phase of the intervertebral disc 100, absorbing nutrients/oxygen/pH buffer 131 from superior diffusion zone 106A and/or inferior diffusion zone 106B of capillaries 107.

DETAILED DESCRIPTION OF THE EMBODIMENTS

Intervertebral discs are avascular (no blood vessels). nutrients/oxygen/pH buffer 131 essential for disc cells are supplied by the capillaries 107 in the vertebral bodies 159 and diffused from superior and inferior endplates 105 into the disc 100, as shown in FIGS. 1 and 2. Blood pH is tightly regulated between 7.35 and 7.45, mainly by the pH buffering bicarbonate dissolved in blood plasma diffused through superior and inferior endplates 105 into the disc 100.

However, depth of diffusion becomes shallow into thick human discs 100. Depth of oxygen diffusion from the endplates 105 is summarized in FIG. 3 (Stairmand J W, Holm S, Urban J P G: Factor influencing oxygen concentration gradients in disc, Spine, Vol. 16, 4, 444-449, 1991). Similarly, depths of glucose diffusion are less than 3 mm from superior and inferior endplates (Maroudas A, Stockwell R A, Nachemson A, Urban J: Factors involved in the nutrition of the human lumbar intervertebral disc: Cellularity and diffusion of glucose in vitro, J. Anat., 120, 113-130, 1975). Human lumbar discs are about 7-12 mm thick. Mid layers of our thick discs 100 suffer severe oxygen and nutritional deficiency. On the other hand, animals have thin discs. Lumbar discs of a large sheep weighing 91 kg (200 pounds) are less than 3 mm thick. Depths of diffusion of oxygen and nutrients seem to be sufficient.

Under anaerobic condition within the mid layer, lactic acid 162 is produced and leaked from the nucleus 128 through fissures 121 to burn surrounding nerves 118, 194 causing persistent back pain, as depicted in FIGS. 4-6. Some patients experience leg pain without visible nerve impingement under MRI or CT. Lactic acid 162 can leak from the nucleus 128 through fissures 121 to spinal nerves 194, causing leg pain as depicted in FIGS. 4-5. Leg pain without visible impingement is commonly called chemical radiculitis.

High lactic acid content in discs correlates with back pain. In fact, dense fibrous scars and adhesions, presumably from lactic acid 162 burn, can be found around nerve roots 194 during spinal surgery [Diamant B, Karlsson J, Nachemson A: Correlation between lactate levels and pH of patients with lumbar rizopathies, Experientia, 24, 1195-6, 1968. Nachemson A: Intradiscal measurements of pH in patients with lumbar rhizopathies. Acta Orthop Scand, 40, 23-43, 1969. Keshari K R, Lotz J C, Link T M, Hu S, Majumdar S, Kurhanewicz J: Lactic acid and proteoglycans as metabolic markers for discogenic back pain, Spine, Vol. 33(3):312-317, 2008].

As we age, calcified layers 108 form and accumulate at the endplates 105, blocking capillaries 107 and further limiting the depth of diffusion of nutrients/oxygen/pH buffer 131 into the disc 100, as shown in FIG. 6. Mid layers of the disc 100 suffer chronic and severe starvation and anaerobic conditions. Disc cells can survive without oxygen, but die without sugars. Nucleus 128 contains glycosaminoglycans or proteoglycans with covalently bonded sugars, essential for retaining water in the disc 100. Degradation of glycosaminoglycans to release sugars for consumption allows disc cells to survive, but initiates compositional and structural change, creating voids 184 and loosely packed nucleus matrix in a degenerated disc 100, as shown in FIG. 7, [Urban J P, Smith S, Fairbank J C T: Nutrition of the Intervertebral Disc, Spine, 29 (23), 2700-2709, 2004. Benneker L M, Heini P F, Alini M, Anderson S E, Ito K: Vertebral endplate marrow contact channel occlusions & intervertebral disc degeneration, Spine V30, 167-173, 2005. Holm S, Maroudas A, Urban J P, Selstam G, Nachemson A: Nutrition of the intervertebral disc: solute transport and metabolism, Connect Tissue Res., 8(2): 101-119, 1981].

Composition Change of the Intervertebral Discs (approximation)

Normal Discs Painful Discs % Change from Normal Discs Glycosamino- 27.4 ± 2.4% 14.1 ± 1.1% −48.5% glycans Collagen 22.6 ± 1.9% 34.8 ± 1.4%   +54% Water content 81.1 ± 0.9% 74.5 ± 1%    −8.1% Acidity pH 7.14 pH 6.65-5.70 [H⁺]: +208% to +2,661% [H⁺]: 7.20 × 10⁻⁸ [H⁺]: 2.23 × 10⁻⁷ to 2.00 × 10⁻⁶ (Reference: Kitano T, Zerwekh J, Usui Y, Edwards M, Flicker P, Mooney V: Biochemical changes associated with the symptomatic human intervertebral disk, Clinical Orthopaedics and Related Research, 293, 372-377, 1993. Scott J E, Bosworth T R, Cribb A M, Taylor J R: The chemical morphology of age-related changes in human intervertebral disc glycosaminoglycans from cervical, thoracic and lumbar nucleus pulposus and annulus fibrosus. J. Anat., 184, 73-82, 1994. Diamant B, Karlsson J, Nachemson A: Correlation between lactate levels and pH of patients with lumbar rizopathies, Experientia, 24, 1195-1196, 1968. Nachemson A: Intradiscal measurements of pH in patients with lumbar rhizopathies, Acta Orthop Scand, 40, 23-43, 1969.)

When glycosaminoglycans diminish, water content and swelling pressure in the nucleus pulposus 128 decrease. The nucleus 128 with reduced swelling pressure can no longer distribute forces evenly against the circumference of the inner annulus 378 to keep the annulus bulging outward. As a result, the inner annulus 378 sags inward while the outer annulus 378 bulges outward, creating annular delamination 114 and weakened annular layers 378, possibly initiating fissure 121 formation depicted in FIGS. 5-6. Holes or vacuoles 184 can be found during dissection of cadaveric discs 100, as shown in FIG. 7. Nucleus pulposi 128 of degenerated discs 100 are usually desiccated, with reduced swelling pressure and decreased capability to sustain compressive loads. The compressive load is thus transferred to the facet joints 129, pressing the inferior articular process 143 against the superior articular process 142 of the facet joint 129, causing strain, wear and/or pain as shown in FIG. 8 (Dunlop R B, Adams M A, Hutton W C: Disc space narrowing and the lumbar facet joints, Journal of Bone and Joint Surgery—British Volume, Vol. 66-B, Issue 5, 706-710, 1984).

A disc 100 with reduced swelling pressure is similar to a flat tire with flexible or flabby side walls. The vertebral body 159 above the soft or flabby disc 100 easily shifts or sways, as shown in FIG. 9. This is commonly called segmental or spinal instability. As shown in FIG. 10, the frequent or excessive movement of the vertebral body 159 strains the facet joints 129, which are responsible for limiting the range of segmental mobility. Patients with spinal instability often use their muscles to guard or support their spines to ease facet pain. As a result, muscle tension and aches arise, but are successfully treated with muscle relaxants. Spinal motions, including compression, torsion, extension, flexion and lateral bending, were measured before and after saline injection into cadaveric discs. Intradiscal saline injections into slow leaking cadaveric discs reduced all spinal motions (Andersson G B J, Schultz A B: Effects of fluid on mechanical properties of intervertebral discs, J. Biomechanics, Vol. 12, 453-458, 1979).

Discography is a common diagnostic technique for identifying or confirming a painful disc 100 before surgical intervention. A spinal needle 102 is guided by a fluoroscope toward the Kambin's Triangle 504 in FIGS. 8 and 11, a posterior-lateral area through which spinal needle 102 can access a lumbar disc 100 safely. The anterior-posterior view in FIG. 12 guides the needle 102 between endplates 105, but does not show the ventral-dorsal location of the needle 102 tip. Before passing the pedicle 278 midway, a lateral fluoroscopic view depicted in FIG. 13 must be taken to ensure the needle 102 is not too dorsal, entering into the epidural space 119. FIG. 13 depicts the lateral fluoroscopic view, showing the needle 101 tip is ventral to the epidural space 119 and can safely enter into the mid layer of the disc 100.

In literature, sizable disc 100 puncturing or laceration accelerates disc degeneration. In non-painful discs 100, a small spinal needle 460 within the spinal needle 102 is used to puncture the disc 100 as shown in FIG. 14. FIG. 15 shows intradiscal injection of X-ray contrast 163, flushing out lactic acid 162 in the disc 100 through fissures 121 to burn the sensory nerve 118, instantaneously causing excruciating pain and confirming specific painful disc 100. For normal or non-painful discs, discography is nearly painless. The spinal needle 102 is not shown in FIG. 15. The spinal needle 102 in FIGS. 11-16 allows joining of diagnostic discography with therapeutic intervention to relieve back pain during the same visit to save time and reduce pain.

After confirming discogenic pain with discography, the needle 102 is advanced into the painful disc 100 over the small spinal needle 460, in FIG. 16. The small spinal needle 460 is replaced with a blunt guide wire 103 in the spinal needle 102 into the disc 100, in FIG. 17. The proximal end of the guide wire 103 is held stationary during withdrawal of the spinal needle 102 from the patient. The proximal end of the guide wire 103 is also held stationary to slide a dilator 220 with a blunt cone head 529 over the guide wire 103 into the disc 100 or tissue, as shown in FIG. 18. A cannula 230 has at least one snagging point 231 and longitudinal lumen 268, as shown in FIG. 19. The snagging point 231 can also be a sharp edge 231 with filament gripping or catching capability. The cannula 230 can have a window 110 opened to the lumen 268 and distal opening. While the proximal end of the dilator 220 is held stationary, the cannula 230 is advanced, sliding over the dilator 220 into the disc 100, as shown in FIG. 20. The guide wire 103 and dilator 220 are removed. A filament needle 101 contains at least one gripper 111 and a longitudinal lumen or opening 269 as shown in FIG. 21. Distal end 126A of a filament 126 is extended from the needle lumen 269, as shown in FIG. 22. The distal end 126A of the filament 126 can be U-shaped. The filament needle 101 with the filament 126 is inserted into the lumen 268 of the cannula 230 into the disc 100, as shown in FIGS. 23-24. A funnel 492 in the proximal end of cannula handle 132 in FIG. 26 is used to facilitate insertion of the filament needle 101 of FIG. 22 into the proximal opening of cannula 230.

During partial withdrawal of the filament needle 101 into the cannula lumen 268, the distal portion 126A or extended portion of the filament 126 is snagged, caught, hooked, retained, trapped, held or grabbed by the snagging point 231 in FIG. 25. As a result, the distal portion 126A or extended portion of the filament 126 remains outside in contact with surrounding tissue in front of the distal end of the cannula 230; and a section of filament 126B, 126C is deposited in the lumen 268 of cannula 230 between the distal ends of the cannula 230 and needle 101. A bobbin 152 holding a spool of filament 126 is attached at the proximal end of a needle handle 130, as shown in FIG. 26. During snagging or holding of the distal portion 126A of the filament 126 and partial withdrawal of the needle 101, additional filament 126 from the bobbin 152 feeds into the lumen 269 of the needle 101. The needle 101 is re-advanced from FIG. 25, pushing or expelling the deposited filament 126B, 126C in front of the needle 101 out the cannula 230 into tissue, as shown in FIGS. 27-28. Excessive withdrawal of the filament needle 101 will deposit a long filament 126B, 126C in front of the filament gripper 111 of the needle 101 within the cannula 230. The long filament 126B, 126C within the cannula 230 can jam the re-advancing needle 101. A latch 495 on a flexible spring or nitinol wire 494 extends from a cannula handle 132 to limit and prevent excessive length or distance of partial withdrawal of the filament needle 101 by stopping the proximal protruded end 501 of the needle handle 130. Hence, length of filament 126B, 126C deposited within the cannula 230 from partial withdrawal of needle 101 is short enough to be pushed or expelled out the cannula 230 by re-advancement of the filament needle 101, as shown in FIGS. 27 and 28. The deposited filament 126B, 126C may also exit through the window 110 of the cannula 230 in FIGS. 19 and 27 to avoid jamming during re-advancement of the needle 101. During insertion of the filament needle 101 in FIG. 22 through the funnel 492 leading into the lumen 268 of the cannula 230, the needle handle 130 slides over the slope 496 of the latch 495 for filament 126 spiraling. FIG. 26 shows a marker 493 on the needle 101. Distal ends of both filament needle 101 and cannula 230 are even, as shown in FIG. 23 or 27, when the marker 493 lines up at the opening of the funnel 492. When the marker 493 enters into the funnel 492, the grippers 111 of the needle 101 are extended outside the cannula 230 to push and pack the filament 126 into tissue.

Major blood vessels, abdominal aorta, inferior vena cava and common iliac arteries, are anterior to the lumbar discs. Distal ends of the devices must remain within the discs 100, confirmable by fluoroscope (X-ray) or markers 493 on the devices. The markers 493 minimize intermittent X-ray exposure to patients and physicians. Markers 493 on the guide wire 103, dilator 220 and filament needle 101 help physician to align distal positions of devices. The following table shows lengths of devices and marker locations to guide implantation of spiraled filament 126 into disc 100 to relieve back and neck pain. Markers 493 in the table are measured from the distal end of the devices. For safety of the patient, length of a guiding device is preferred to be longer than the subsequent device, so that the proximal end of the guiding device can be held stationary during insertion of the subsequent device into patient.

Length, Marker 1, Marker 2, Device OD, mm ID, mm mm mm mm Spinal 1.27 0.84 172 needle 102 Small spinal 0.51 0.25 226 needle 460 Guide wire 0.81 492 172 338 103 Dilator 220 1.83 1.00 338 185 Cannula 230 2.41 1.97 185 Filament 1.83 1.52 230 185 needle 101 Filament 126 0.67-0.77 900 double strands Distal ends of spinal needle 102 and guide wire or tube 103 are even, when Marker 1 of the guide wire 103 is at the proximal end of the spinal needle 102, as shown in FIG. 17. Distal ends of the dilator 220 and guide wire 103 are even, when Marker 2 of the guide wire 103 is at the proximal end of the dilator 220, as shown in FIG. 18. Distal ends of cannula 230 and dilator 220 are even, when Marker 1 of the dilator 220 is at the proximal end of cannula 230, as shown in FIG. 20. Distal ends of the cannula 230 and filament needle 101 are even, when Marker 1 of the needle 101 is at the proximal end of the cannula 230, as shown in FIG. 24.

Annulus 378 of the disc 100 is made mainly with layers of collagen. Layers of collagen form a net-like matrix. Spinal needles 102 or 460 with single sharp tips have no problem puncturing through the net-like collagen matrix of the annulus 378. On the other hand, the cannula 230 and filament needle 101 have multiple sharp points 231, 111 at the distal ends, as forks. The cannula 230 contains indentations 113 between snagging points 231 in FIG. 19; and filament needle 101 contains indentations 120 between grippers 111 in FIGS. 21-22. The indentations 113, 120 are trapped by the net-like collagen matrix with no annular penetration capability to prevent possibility of injuring blood vessels anterior to the discs 100. The guide wire or tube 103 and dilator 220 are blunt and have little capability of penetrating annulus 378 to ensure safety of the patient.

During pushing and rotation of the filament needle 101, at least one of the grippers 111 grabs and spins the extended filament 126B, 126C burrowing and spiraling into nucleus 128, fissure 121, void 184 or soft tissue, as shown in FIG. 29. Spiraling of the extended filament 126 is made possible by the twisting gripper 111 and friction between the extended filament 126 and tissue. A knot-like spiraled filament 126 is formed due to rotation of the filament needle 101, as shown in FIG. 30. The filament needle 101 can also advance or extend beyond the distal end of the cannula 230 to push, pack, fill, load, cram or stuff the expelled filament 126, burrowing into nucleus 128, void 184, fissure 121 or tissue, as shown in FIG. 31. The filament needle 101 is partially withdrawn again; the extended filament 126 is caught again by the snagging point 231 of the cannula 230, as shown in FIG. 32. In fact, the initial spiraled filament 126 also acts as an anchor outside the distal end of the cannula 230; partial withdrawal of the needle 101 deposits or loads additional filament 126B, 126C within the cannula 230 between distal ends of cannula 230 and needle 101. The filament needle 101 is re-advanced, pushing or expelling the additional filament 126 out of the cannula 230 into tissue 31, as shown in FIG. 33. Rotations of the needle 101 form another spiraled filament 126, linking to the previously spiraled filament 126, as shown in FIG. 34. Same direction of needle 101 rotations is preferred. Rotation and pushing of the needle 101 help the spiraled filament 126 to seek, burrow and fill void 184, gap, fissure 121, vacancy, weak spot, opening, cavity or soft spot. The steps of needle 101 withdrawal, re-advancement, rotation and pushing, are repeated to build, fill, bulk, pack, fortify, load or solidify the tissue with multiple inter-connecting spirals of filament 126, as shown in FIGS. 35-36. Multiple spirals or coils of filament 126 are formed, packed or inserted individually to be shape conforming, malleable and/or resilient in voids 184, yet inter-connected to prevent or minimize migration from tissue. Rotation and pushing of the needle 101 drive the spirals of filament 126 from the lumen 269 of the needle 101 to seek, fill and pack the distal, lateral and/or proximal space in tissue. The spirals of filament 126 are formed in multiple axes. Tightness of the spiraled filament 126 is determined by number of rotations and intensity of pushing of the needle 101. The spiral filament 126 can be as tight as a suture knot. Fewer rotations and/or gentle pushing of the needle 101 make soft spirals of filament 126. Number of rotations and pushing intensity of the needle 101 can be alternate to allow variations in firmness or density of filament spirals 126 within repaired tissue. It is possible to sequentially and partially withdraw the cannula 230 from tissue to provide additional head or distal space for packing additional spirals of filament 126 in front of the cannula 230 into the tissue.

Needle handle 130 and cannula handle 132 are dumbbell shape. The needle handle 130 has a protruded proximal end 501 and a protruded distal end 500 to facilitate withdrawal and advancement of the needle 101, as shown in FIG. 26. The needle handle 130 also contains gripping or friction ridges 502 to facilitate rotation of the needle 101. The cannula handle 132 has a protruded proximal end 499 and a protruded distal end 498 to facilitate withdrawal and advancement of the cannula 230. When the tissue is full with spirals of filament 126, advancement of the needle 101 becomes difficult. The cannula 230 can also be slightly and sequentially withdrawn from tissue, to pack or accumulate additional spirals of filament 126 distal to the cannula 230. A metering device can be attached to the spool of filament 126 on the bobbin 152 to monitor length of filament 126 dispensed into patient. When the tissue is packed with spirals of filament 126, the filament needle 101 and cannula 230 are withdrawn from tissue. In the event of disc 100 repair, the extended filament 126 is cut above the skin 505, as shown in FIG. 37. The proximal portions of filament 126B, 126C are tucked beneath the skin 505 with a long and thin forceps 525, as shown in FIG. 38. The amount of implanted filament 126 is selectable, controllable, limitable or regulateable by the physician.

In summary, the cannula 230 and filament needle 101 work together to spiral the filament 126 or fluid absorbing conduit 126 to bulk or shim the tissue. The cannula 230 with snagging points 231 prevents the extended filament 126A from retrieving or retracting into the lumen 269 of the filament needle 101. Additional filament 126 is advanced by either withdrawal/re-advancement of the needle 101 or by a filament advancer 526 within the needle 101. Rotation of the needle 101 with grippers 111 holds and spirals the filament 126 burrowing into voids 184 and fissure 121. The filament spiral 126 is individually formed by spatial allowance of the tissue, and not spiraling over a spindle, axle, axis or needle. Filament 126 spiraling driven by the rotating needle 101 is space seeking, filling, fitting or conforming to fortify, bulk, fill, cushion, shim or repair the tissue. Pushing of the needle 101 further packs the spiraled filament 126 to bulk the tissue.

PCT/US2011/000007, WO/2011/082390 (Internal and external disc shunts alleviate back pain, by Jeffrey E. Yeung and Teresa Yeung, filed on 3 Jan. 2011) contains a U-shaped shunt 126 partly within and partly outside a needle 101, and a sleeve 220 sliding over the needle 101. During rotation of the needle 101, the outside draping shunt 126 spirals over the needle 101 shaft. The sleeve 220 is then advanced distally to strip the spiraled shunt 126 off the shaft of the needle 101, pushing the spiraled shunt 126 into the nucleus of the intervertebral disc 100. The sleeve 220 is retrieved to the proximal position. Another spiral of shunt 126 is formed by rotation of the needle 101, the sleeve 220 is advanced again to strip the spiraled shunt 126 off the needle 101 into the nucleus. The process of needle 101 rotation, sleeve 220 advancement and sleeve 220 retrieval are repeated to form spirals of shunt 126 within the disc 100. However, many problems occurred during usages of this device in clinical study. Due to friction between disc 100 and sleeve 220, advancement of the sleeve 220 for stripping the spiraled shunt 126 from the needle 101 is very difficult. Significant force is required to advance the sleeve 220, which adds significant risks of puncturing through the disc 100 and rupturing major blood vessels anterior to the disc 100. In addition, due to direct contact of the sleeve 220 with the painful disc 100, patient feels extreme pain during advancement of the sleeve 220 to dislodge the spiraled shunt 126 on the needle 110. Significant pain is endured during multiple dislodgements of shunt spirals 126. Fortunately, the patient experienced pain relief within a week due to efficacy of the disc shunt 126.

Unlike PCT/US2011/000007, WO/2011/082390, the cannula 230 in this application is stationary during implantation of the filament 126 into disc 100 or tissue. The filament needle 101 slides freely within the cannula 230 without risk to the patient or causing pain. The spiral of filament 126 is driven by the grippers 111 and formed distal to the rotating needle 101, capable of burrowing, drilling, packing, wiggling, building, dilating, wedging or shimming into voids 184, fissure 121 or tissue. Unlike PCT/US2011/000007, tissue burrowing of the distal forming filament spiral 126 in this application is particularly effective, implanting deep into tissue, as shown in FIG. 31, embedding, filling, packing and bulking the tissue as shown in FIG. 36. On the other hand, the spiraled filament 126 in PCT/US2011/000007, WO/2011/082390 is already formed on the needle 101 shaft, which may not fit into small voids 184 or fissures 121.

Fluid flows from low to high osmotic pressure according to the law of physics. Osmotic pressure of fluid in muscle 193 is approximately 250-300 mOsm/liter; intervertebral disc 100 is 300-400 mOsm/liter. Through the difference between osmotic pressures, the connecting filament 126 draws fluid from muscle 193 to hydrate the desiccated nucleus 128 without a pump, as shown in FIG. 39.

In-vitro study, the filament 126 was implanted into sheep discs 100 (430 mOsm/liter) and human cadaver discs 100 (300-400 mOsm/liter) of various degenerative levels, Thompson Grade 0-4. The discs 100 with filaments 126 were submerged in saline with blue dye (300 mOsm/liter). Dissection of the discs 100 showed blue saline permeation into the nuclei 128, confirming fluid flows from low to high osmotic pressure.

Another filament 126 was implanted through a muscle into a sheep disc 100. The sheep muscle 193 was saturated with iopamidol (contrast agent with blue dye, 545 mOsm/l). The blue iopamidol did not permeate through the filament 126 into the sheep disc 100 (430 mOsm/liter). In fact the dissected disc 100 looked desiccated; fluid within the sheep disc 100 was probably drawn into the muscle 193 infused with 545 mOsm/liter blue iopamidol through the filament 126. The experiment was repeated with diluted blue iopamidol solution (150 mOsm/liter). The diluted iopamidol solution saturated the muscle 193 and permeated through the filament 126 into the sheep disc 100 visible and traceable from muscle 193 to nucleus 128 under CT. Dissection confirmed permeation of the diluted blue iopamidol into the nucleus 128 of the sheep disc 100. Again, fluid flows from low to high osmotic pressure through the filament 126.

Sheep discs were implanted with filaments 126 and submerged in pork blood (about 320 mOsm/liter). Dissection of the discs 100 showed permeation of pork blood through the filament 126 into the nuclei of the sheep discs 100 (430 mOsm/liter). Gradient of pH is formed in the disc 100 due to shallow diffusion of nutrients/oxygen/pH buffer 131 from the capillaries 107 at the endplates 105. The superior 106A and inferior 106B diffusion zones are approximately 0-2 mm from the superior or inferior endplates 105. The pH in the superior 106A and inferior 106B diffusion zones is neutral. Acidity increases at the mid layer of the disc 100, where chronic deprivation of oxygen, nutrients and pH buffer occurs. FIG. 40 shows a longitudinal view of a filament 126 filled disc 100 with calcified layers 108 accumulated over the endplate 105. The hydrophilic spiraled filament 126 or fluid absorbing conduit 126 reaches, locates, resides or contacts at least one of the superior 106A and inferior 106B diffusion zones, drawing and transporting nutrients/oxygen/pH buffer 131 to neutralize lactic acid 162 and nourish cells in the mid layer of the disc 100. As a result, lactic acid 162 burn is minimized and back pain is relieved. In essence, the spiraled filament 126 or fluid absorbing conduit 126 bridges, links or transports fluid between source of nutrients/oxygen/pH buffer 131 and mid layer of the disc 100 to treat the etiology and symptom of back pain. Furthermore, oxygen 131 from the muscle 193, superior 106A and inferior 106B diffusion zones converts anaerobic conditions into aerobic within the mid layer of the disc 100 to further reduce production of lactic acid 162 and relieve back pain.

The fluid absorbing conduit 126 can be a filament 126; which can be further identified as internal conduit 126 and external conduit 126. The conduit 126 in the disc 100 can be called the conduit-implanted disc 100 to form as internal conduit 126 between superior diffusion zone 106A and inferior diffusion zone 106B. The fluid absorbing conduit 126 extending from disc 100 to body circulation or muscle 193 is called external conduit 126. The fluid absorbing filament 126 is a fluid-transferring or delivery device, inserted into the nucleus 128 of a degenerated disc 100. Due to relaxation and compression of the disc 100 from daily activities of the patient, the fluid absorbing conduit 126 in the disc 100 facilitates transport of nutrients/oxygen/pH buffer 131 through out the disc 100. During relaxation, nutrients/oxygen/pH buffer 131 from diffusion zones 106A, 106B are absorbed by the internal conduit 126, and nutrients/oxygen/pH buffer 131 in muscle 193 are drawn through the external conduit 126. During compression, nutrients/oxygen/pH buffer 131 in the conduit 126 are expelled to neutralize lactic acid 162 and fed to disc cells in the mid layer of the disc 100. Essentially, both diffusion zones 106A, 106B are expanded to cover the mid layer or acidic layer of the disc 100. Hence, fluid leaking from the fissure 121 is pH neutral or near pH neutral to alleviate back pain, as shown in FIG. 40. Fluid transport or distribution is made possible by soft and pliable spirals of fluid absorbing conduit 126 or filament 126 as internal conduit 126 with hydrophilic and malleable properties, absorbing and delivering nutrients/oxygen/pH buffer 131 within the avascular disc 100. Fluid flow through the fluid absorbing conduit 126 is dynamic and continuous to rebuild disc matrix for disc regeneration.

Nutrients/oxygen/pH buffers 131 are diffused from the capillaries 107 at the endplates 105 into the nutrient-poor avascular disc 100, as shown in FIG. 40. Diffusion is concentration related; solutes move from high to low concentration, from capillaries 107 into diffusion zones 106A, 106B. Withdrawal of nutrients/oxygen/pH buffers 131 by the internal fluid absorbing conduit 126 leads to additional diffusion of nutrients/oxygen/pH buffers 131 from capillaries 107 and vascular buds. The net supply of nutrients/oxygen/pH buffer solutes 131 into the disc 100 will increase with implantation of the internal conduit 126 as shown in FIG. 40. Distribution of nutrients/oxygen/pH buffer 131 is expanded by the internal conduit 126 covering or permeating the full-thickness of the intervertebral disc 100 to neutralize lactic acid 162, nourish starving disc cells 277 and rebuild disc matrix to sustain compressive loading of the disc 100.

Depending on the amount of calcified layers 108 blocking the capillaries 107 and vascular buds at the endplates 105, depths or thicknesses of superior 106A and inferior 106B diffusion zones of nutrients/oxygen/pH buffer 131 from body circulation into disc 100 are between 0 and 5 mm from the superior and inferior endplates 105. For degenerated and/or painful disc 100, depths or thicknesses of superior 106A and inferior 106B diffusion zones into disc 100 are likely between 0 and 3 mm from the superior and inferior endplates 105, as depicted in FIG. 6. The internal disc conduit 126 or fluid absorbing conduit 126 should reach at least one, but preferably both superior 106A and inferior 106B diffusion zones, as depicted in FIGS. 40, 89-91. Deployment, formation or location of the spiraled filament 126 or fluid absorbing conduit 126 is between 0 and 5 mm from the superior and/or inferior endplates 105 as depicted in FIGS. 40, 89-91, but preferred between 0 and 3 mm from the superior and/or inferior endplates 105 to draw nutrients/oxygen/pH buffer 131 from fluid of body circulation into the mid-layer of the disc 100. As the result, pH buffer 131 from body circulation neutralizes the lactic acid 162 to relieve discogenic pain. Oxygen 131 from body circulation inhibits anaerobic production of lactic acid 162 and hypoxic inflammation to further relieve discogenic pain. Nutrients 131 from body circulation feed disc cells to make new disc matrix to regenerate the degenerated disc 100. Furthermore, similar to deep wound, hollow disc 100 from degeneration never heals. The filament 126 or fluid absorbing conduit 126 also serves as a tissue filler and scaffold 126, packing within the hollow disc 100 for cellular and new disc matrix attachment to facilitate disc 100 regeneration.

Due to avascular nature, intervertebral disc 100 is immuno-isolated. In-vivo sheep study, there was no tissue response within the discs 100 to nylon filament 126 after 1, 3, 6, 12 and 30 months, using H&E histology staining. No fibrotic encapsulation over the nylon filament 126 was observed within the discs 100. Similarly, there was no noticeable inflammatory reaction to the nylon filament 126 in a human pilot clinical study in 1 week, 3, 6, 12 and 24 months. Internal transport of nutrients/oxygen/pH buffer 131 from superior 106A and/or inferior 106B diffusion zones continues without hindrance of fibrotic encapsulation over the filament 126 or fluid absorbing conduit 126 within the intervertebral disc 100.

The spirals of filament 126 or fluid absorbing conduit 126 provide bulk, shimming, filling, cushion, mass, wedging or fortification within the disc 100 to elevate, raise, lift, increase or sustain disc 100 height as indicated by arrows in FIGS. 40-41. Spirals of filament 126 or fluid absorbing conduit 126 bulks up the nucleus 128 to elevate or support disc height for sustaining axial compression, stiffen the disc 100 for reducing spinal instability, and/or lift the inferior articular process 143 of the facet joint 129 to reduce facet pain, as shown in FIG. 41.

Cervical discs 100 are thinner than lumbar discs 100. Flattening of cervical disc 100 from degeneration quickly leads to facet loading, erosion and pain, affecting up to 55% neck pain patients. Shimming with the spirals of filament 126 or fluid absorbing conduit 126 thickens or increases cervical disc 100 height to instantly relieve facet pain, as shown in FIGS. 40-41, 89. In addition, approximately 20% neck pain patients suffer from discogenic pain from lactic acid burn. Re-establishing fluid transport between body circulation and the avascular disc 100 through the spirals filament 126 or fluid absorbing conduit 126 also relieve discogenic pain of the cervical disc 100 as well.

Nutrients/oxygen/pH buffer 131 transporting through the filament 126 feed cells 277 to produce biosynthetic molecules, which can be glycosaminoglycans, proteoglycans, collagen or disc matrix, as shown in FIG. 42. Cells 277, nutrients/oxygen/pH buffer/therapeutic agent 131 can also be intradiscally injected into the disc 100 containing the spirals of filament 126 or fluid absorbing conduit 126 as shown in FIGS. 43 and 46, to expedite disc 100 regeneration, lifting the inferior articular process 143 of the facet joint 129 to unload and relieve pain in the facet joints 129 as shown in FIG. 41. Nutrients 131 include sulfate, amino acids, sugars and/or minerals. Therapeutic agent 131 includes antibiotic, nonsteroidal anti-inflammatory drug, analgesic, anti-inflammatory steroid, anesthetic, muscle relaxant, antacid, alkaline agent, growth factor, anti-depressant, calcium channel blocker or cells.

Physician can feel the fullness of the disc 100 during advancement of the needle 101 in FIG. 31. When the disc 100 is full or nearly full with the filament 126 or fluid absorbing conduit 126, the marker 493 of the filament needle 101 cannot advance into the cannula 230 or the funnel 492 of the cannula 230, as depicted in FIG. 26. The cannula 230 can be slightly or partially withdrawn to make head space in front of the cannula 230, while the distal end of the cannula 230 remains in the disc 100. The filament 126 extended from the proximal end of the filament needle 101 between the bobbin 152 and filament needle handle 130, as depicted in FIG. 26, can be cut. The filament 126 or fluid absorbing conduit 126 in the needle 101 is implanted or advanced into the head space in front of the cannula 230 as depicted in FIGS. 27, 29-36. The filament needle 101 or fluid absorbing conduit needle 101 is withdrawn from the cannula as shown in FIG. 44. The entire filament 126 or fluid absorbing conduit 126 is implanted within the disc 100 as shown in FIG. 45.

Nutrients, pH buffer, therapeutic agent 131 or cells 277 in a syringe 276 and needle 460 can be injected into the disc 100 through the cannula 230 after implanting the filament 126 or fluid absorbing conduit 126 as shown in FIG. 46. Nutrients 131 include sulfate, amino acids, sugars and/or minerals. Therapeutic agent 131 includes antibiotic, nonsteroidal anti-inflammatory drug, analgesic, anti-inflammatory steroid, anesthetic, muscle relaxant, antacid, alkaline agent, growth factor, anti-depressant, calcium channel blocker or cells.

Lower lumbar L5-S1 disc 100A and L4-5 disc 100B are shielded by a pair of iliac crests 140, as shown in FIG. 47. The straight spinal needle 102 enters superiorly over the iliac crest 140 at an angle, as shown in FIG. 48, difficult or even impossible to deliver the filament 126 or fluid absorbing conduit 126 into central nucleus 128 of the disc 100.

FIG. 49 shows an elastically curved cannula 230 leading the filament needle 101 into the nucleus 128 of a degenerated disc 100. The elastically curved cannula 230 is resiliently straightened by sliding over the rigid dilator 220 into the annulus 378 of the disc 100. Then, the dilator 220 is partially withdrawn while holding the cannula stationary. The cannula 230 resumes the curvature and advances into the loosely packed nucleus 128. After confirming distal location of the curved cannula 230 by fluoroscope, the filament needle 101 in FIG. 22 replaces the dilator 220 for filament 126 spiraling, similar to FIGS. 25, 27-36. The cannula 230 and needle 101 can be made with elastic material, including nickel titanium alloy for shaped memory and super elasticity.

In summary, insertion of the spiraled filament 126 or fluid absorbing conduit 126 into disc 100 increases nutrients/oxygen/pH buffer 131 from muscle 193 and/or diffusion zones 106A, 106B to reduce lactic acid 162 burn and feed cells. The spiraled filament 126 or fluid absorbing conduit 126 also adds bulk and cushion to treat, reduce or relieve spinal instability and facet pain.

The filament 126 or fluid absorbing conduit 126 for disc 100 repair is hydrophilic with measurable characteristics under ambient temperature and pressure for transporting and retaining fluid to relieve pain and/or regenerate the degenerated disc 100. After saturation in water, the fluid absorbing conduit 126 gains weight between 10% and 500% by absorbing water within the matrix of the fluid absorbing conduit 126. A healthy human disc 100 contains 80% water. The preferred water absorbency after water saturation is between 30% and 120%. The fluid absorbing conduit 126 can have pore sizes between 1 nano-meter and 500 micro-meters, serving as water retaining pockets or water transporting channels. Pores 124 of the fluid absorbing conduit 126 also function as scaffolding or housing for cell 277 attachment and cellular proliferation, as shown in FIG. 42. Water contact angle on the fluid absorbing conduit 126 is between 0 and 60 degrees. The preferred water contact angle of the fluid absorbing conduit 126 is between 0 and 30 degrees. Height of capillary action for drawing saline up the fluid absorbing conduit 126 is between 0.5 and 120 cm. The preferred height of capillary action of drawing saline is between 1 and 60 cm. Height of capillary action for drawing pork blood up the fluid absorbing conduit 126 is between 0.5 and 50 cm. The preferred height of capillary action for drawing pork blood up the fluid absorbing conduit 126 is between 1 cm and 25 cm. Saline siphoning transport rate through the fluid absorbing conduit 126 is between 0.1 and 10 cc per 8 hours in a humidity chamber. Human lumbar disc 100 loses between about 0.5 and 1.5 cc fluid per day due to compression. The saline siphoning transport rate through the fluid absorbing conduit 126 is preferred between 0.5 and 5 cc per 8 hours in a humidity chamber. Pork blood siphoning transport rate through the fluid absorbing conduit 126 is between 0.1 and 10 cc per 8 hours in a humidity chamber. The pork blood siphoning transport rate through the fluid absorbing conduit 126 is preferred between 0.5 and 3 cc per 8 hours in a humidity chamber.

The fluid absorbing conduit 126 used in the sheep and human clinical studies have the following physical properties under ambient temperature and pressure: (1) weight gain 80% after water saturation, (2) water contact angle zero degree, (3) height of capillary action 11 cm with pork blood, 40 cm with saline with blue dye, and (4) rate of siphoning pork blood 1.656 +1-0.013 cc per 8 hours in a humidity chamber.

Average lactic acid concentration in painful lumbar disc 100 is about 14.5 mM, 15 cc or less in volume (Diamant B, Karlsson J, Nachemson A: Correlation between lactate levels and pH of patients with lumbar rizopathies. Experientia, 24, 1195-1196, 1968). An in-vitro study was conducted to show instant lactic acid neutralization by blood plasma. The spiraled filament 126 was formed within, and then extracted from a fresh portion of beef Blood plasma absorbed in the spiraled filament 126 instantly neutralized 42% of the 14.5 mM, 15 cc of lactic acid solution, measurable by a pH meter.

Approximately 85% back pain patients show no nerve impingement under MRI or CT. A patient without nerve impingement suffered chronic back pain with visual analog score 8-9 out of 10 (most severe), and leg pain with visual analog score 8. Five days after implantation of the filament 126, the visual analog score dropped to 2.5 for her back pain, but the visual analog score persisted at 8 for leg pain. In the 5.5-month follow-up, the visual analog score dropped to 2.0 for her back pain, and visual analog score dropped from 8 to zero for leg pain. Quick back pain relief may be contributed to instant lactic acid 162 neutralization by fluid from body circulation of the patient to relieve acid burning of the adjacent sensory nerves 118. Leg pain may be caused by acid scaring of the spinal nerve 194 and chemical radiculitis, which takes time to heal and relieve the pain. In human clinical study, the outer diameters of the needle 101 and cannula 230 are only 1.83 and 2.41 mm respectively. The outer diameter of the fluid absorbing conduit 126 is 0.55-0.77 mm.

Urinary incontinence is common among women, especially after multiple pregnancies and vaginal deliveries. Major urethral sphincteric action is operated by smooth muscle 532 at the bladder neck 519. FIG. 50 shows a normal and narrow bladder neck 519 of a woman with urinary control. The smooth muscle 532 controls opening and closure of the urethral lumen 517 lined with mucosa 533. During pregnancy, the baby presses against the bladder 518 and the urethra 516 for months. The downward compression flattens and widens the smooth muscle 532 and urethral lumen 517 of the bladder neck 519, as shown in FIG. 51. A widened lumen 517 at the bladder neck 519 is beyond the range of sphincteric closure of the smooth muscle 532 for coaptation of mucosa 533 in urethral lumen 517. As a result, stress urinary incontinence occurs during increased abdominal pressure from coughing, sneezing, laughing or even standing. In surgical intervention for stress incontinence, the vagina 520 is pulled and fastened to ligaments anteriorly, to support and push forward the posterior wall 524 of the bladder neck 519, narrowing the urethral lumen 517 for coaptation of urethral mucosa 533 during sphincteric action.

A needle 460 within a cone-head dilator 220 in FIG. 52 is inserted into urethral smooth muscle 532 of the bladder neck 519 under cystoscopic or ultrasound guidance. An echogenic gel can be injected through the needle 460 to confirm location of the needle 460 tip within the urethral muscle 532. The cone-head dilator 220 slides over the needle 460 into the urethral muscle 532. The needle 460 is withdrawn. Addition echogenic gel can be injected through the removable luer lock 530 to ensure location of the dilator 220 tip within the urethral muscle 532. The luer lock 530 is removed to prepare for repair. Similar to disc 100 repair, a cannula 230 slides over the dilator 220 into the urethral muscle 532. The dilator 220 is replaced with a filament needle 101 loaded with filament 126 within the cannula 230, as shown in FIG. 23. Spiraled filament 126 in FIG. 53 is created by withdrawal, advancement, rotation and pushing of the filament needle 101, as shown in FIGS. 25, 27 and 29-35. FIG. 54 shows a cross-sectional view of the urethra 516 with a widened urethral lumen 517 and initial spiraled filament 126 formed within the smooth muscle 532 of the posterior wall 524 of the urethra 516. FIG. 55 shows bulking, enlargement or filling of the urethral smooth muscle 532 with spirals of filament 126 at the posterior wall 524 to encroach or extend into the space of urethral lumen 517, resulting in size reduction of the urethral lumen 517 to facilitate coaptation of urethral mucosa 533 during sphincteric action of the urethral muscle 532. Multiple locations of spiraled filaments 126 can be implanted in urethral muscle 532 to further narrowing the urethral lumen 517, as shown in FIG. 56. For bulking of urethra 516, no filament 126 should be extended into the lumen 517 to avoid infiltration of bacteria into the smooth urethral muscle 532. When closure of urethral lumen 517 with bulking of the filament 126 seems adequate through the cystoscope, the filament 126 between the proximal end 501 of needle handle 130 and bobbin 152 in FIG. 26 is cut. Spiraling of the filament 126 continues with withdrawal, re-advancement and rotation of the needle 101 to completely spiral the remaining filament 126 in needle 101 into urethral muscle 532. The amount of implanted filament 126 is selectable, controllable, limitable or regulateable by the physician. The filament 126 can be a nylon, polypropylene or biodegradable mono-filament suture with some stiffness or shape memory. Coiling or spiraling of the shape memory filament 126 expands within tissue to provide elastic bulking or expansion to enhance the backboard support and sphincteric action of the urethra 516. FIG. 57 shows narrowing of the bladder neck 519 by spirals of filament 126 cushioning, bulking or supporting tissue between the vagina 520 and urethral lumen 517 to relieve stress urinary incontinence and regain sphincteric control.

Gel-like bulking agent has been injected into fecal sphincteric muscle to treat fecal incontinence, but feces can be substantially firm and large to flatten and nullify bulking of the gel-like agent. On the other hand, the elastic and shape-memory spirals of filament 126 are inter-connected to prevent flattening, migration or dislocation, to maintain fecal sphincteric bulking and control, similar to urethral bulking in FIGS. 53-56.

The filament 126 can be a suture 126. The suture 126 spiraling device can also be used to spiral and pack suture 126 under skin to fill indentations from acne scar or cosmetic defect. The spirals of suture 126 at the distal end can also be used as a suture anchor deep within tissue. The proximal end of the suture 126 can be threaded with a tissue repairing needle for tissue fastening through micro-invasive procedure, such as face lift and other suture repair.

The filament 126 or fluid absorbing conduit 126 can expand or swell during hydration in body fluid. The swelled filament 126 adds size or mass within tissue to enhance bulking or efficacy of the spirals of filament 126 or fluid absorbing conduit 126. The filament 126 can also be coated with a hydrophilic or swelling agent, such as polyethylene glycol, collagen, hyaluronic acid or other, for expansion.

The dilator 220 in FIG. 52 can be substituted with the cannula 230 connecting to a luer lock 531 at the proximal end for injection of echogenic liquid. After needle 460 puncturing into urethral muscle 532, the cannula 230 is advanced by sliding over the needle 460 into urethral muscle 532. The needle 460 is withdrawn. Echogenic gel or liquid can be injected through the cannula 230 to confirm distal location of the cannula 230 in urethral muscle 532. Since the cannula 230 has no tissue puncturing capability, injection of echogenic gel for location confirmation may not be necessary. The filament needle 101 is inserted into the cannula 230 for spiraling filament 126.

A knot 463 can be tied at the distal portion 126A of the filament 126 to prevent retrieval of the filament 126 into the lumen 269 of the needle 101, as shown in FIG. 58. The knot 463 also facilitates catching or hooking by the snagging point 231 of the cannula 230, further improved from FIG. 25. The U-strand of the filament 126 can be divided into distal portion 126A and proximal portions 126B and 126C. A proximal portion 126B of the filament 126 can drape outside, while another proximal portion 126C of the filament 126 can be inserted in the needle 101 as shown in FIG. 59. A single stranded filament 126 can be inserted into the needle 101, as shown in FIG. 60. The single stranded filament 126 can also be snagged by the snagging points 231 of the cannula 230 and rotated into spiraled filament 126. A knot 463 is tied at the distal portion 126A to prevent retrieval of the single stranded filament 126 into the lumen 269 of the needle 101, as shown in FIG. 60. An anchor 462 can be attached at the distal end of the filament 126, as shown in FIG. 61. The anchor 462 can be made with a biodegradable material or tablet of a pH buffer, nutrients or therapeutic agent 131. The anchor 462 can also be a toggle 462, a protrusion 462 or latch 462.

The filament gripper 111 can be a cross bar 111 as shown in FIG. 62. The filament 126 loops over the cross bar 111, as shown in FIG. 63, for insertion into the cannula 230. The cross bar 111 can be a longitudinal plane, dividing the cylindrical lumen 269 of the needle 101 into two semi-cylindrical lumens 269, as shown in FIG. 64. The cross bar 111 or cross plane 111 can tightly pack the spiraled filament 126 into tissue. The cross bar 111 can be extended by two extension bars 112 as shown in FIG. 65. The filament 126 loops over the extended cross bar 111, as shown in FIG. 66. The extended cross bar 111 can also be extended into a cross plane 111, dividing into two semi-cylindrical lumens 269. Filament grippers 111 can be cross stubs 111 as shown in FIG. 67. The cross stubs 111 can also be two longitudinal stubs length-wise through the lumen 269, as shown in FIG. 68.

Loading filament 126 from the bobbin 152 into proximal lumen 269 of the needle 101 is driven by holding the distal end 126A of the filament 126 and withdrawing the needle 101, as shown in FIGS. 25, 26 and 32. A filament advancer 526 can be manually used or motorized to advance the filament 126 without needle 101 withdrawal. The filament advancer 526 contains a stem 527 attaching resiliently collapsible barbs 528 pointing distally, as shown in FIG. 69. The resiliently collapsible barbs 528 have a closed and open positions. In the closed position, the distal ends of the resiliently collapsible barbs 528 approximate the stem 527, as shown in solid lines of FIG. 70. In the open position, the distal ends of the resiliently collapsible barbs 528 depart or move outward from the stem 527, as shown in dashed lines of FIG. 70. In operation within tissue, distal end of the filament advancer 526 and the resiliently collapsible barbs 528 are mostly concealed and operated within the lumen 269 of the needle 101. During distal movement of the filament advancer 526, the collapsible barbs 528 are in the open positions to grip, puncture, insert, hold, grab, attach, engage, hook or latch on the filament 126, moving the filament 126 distally. During proximal movement of the filament advancer 526, the resiliently collapsible barbs 528 release the engagement with the filament 126 and retract, retrieve or collapse into the closed positions to approximating the stem 527. The collapsible barbs 528 are elastic or flexible to grip and release the filament 126 during cyclical distal-proximal movement of the stem 527 or filament advancer 526. The collapsible barbs 528 are spaced out along the stem 527. The axial or vertical view of the filament advancer 526 in FIG. 71 shows orientations of the resiliently collapsible barb 528 approximately 120 degrees apart. FIG. 72 shows the collapsible barbs 528 approximately 90 degrees apart.

The filament 126 can also be advanced by a manually driven or motorized rotational auger 526 as filament advancer 526 within the lumen 269 of the needle 101, as shown in FIG. 73. The auger 526 contains a stem 527 and screw-like or helical thread 528 to engage, convey or propel the filament 126 out the needle 101. In operation within tissue, distal end of the filament advancer 526 and the screw-like thread 528 are concealed and operated within the lumen 269 of the needle 101.

The needle lumen 269 can be non-circular shape. Cross-section of the lumen 269 can contain two connecting circular lumens 269, one for housing the filament advancer 526 and the other for housing the filament 126, similar configuration as FIG. 74. The opening between the two connecting circular lumens 269 allows the collapsible barbs 528 or helical thread 528 to extend and engage with the filament 126.

The motorized speed of the resiliently collapsible barbs 528 and screw-like thread 528 can be controlled by a foot pedal. During high torque, a torque sensor initiates reduction or stopping of the motor. The motorized filament advancer 526 saves surgical time and allows physician to concentrate on needle 101 rotation and pushing to pack filament 126 for repairing tissue. The resiliently collapsible barbs 528 and the screw-like thread 528 can be called the filament engager 528 of the filament advancer 526.

FIG. 75 shows a cannula 230 with multiple snagging points 231 to facilitate holding on the filament 126. FIG. 76 shows a large window 110 for filament 126 to protrude during needle re-advancement to prevent jamming. The window 110 is open to a snagging point 231. FIG. 77 shows elastically curved or inward bending of snagging points 231 of the cannula 230 to facilitate trapping or hooking of the extended filament 126 in FIGS. 22-25, 27-28, 32 from the needle 101. The cannula 230 with elastically curved snagging points 231 can be made with nickel-titanium alloy or nitinol. During advancement of the filament needle 101, the elastically curved snagging points 231 resiliently open or straighten to allow passing of the needle 101 and the extended filament 126. The elastically curved snagging points 231 provide inward grip to trap, catch or hook the extended filament 126, similar to the result of FIGS. 25 and 32. Other elastically curved snagging points 231 of the cannula 230 are shown in FIG. 78. The snagging points 231 can be elastically curved walls or gates 231 at the distal end of the cannula 230 in FIG. 79 to hook or trap the extended filament 126 from the needle 101. FIG. 80 shows a cross-sectional view of the inward bending or elastically curved gates 231, restricting the distal lumen 268 of the cannula 230. The elastic snagging point 231 can be called a spring biased arm 231.

Flexible filament 126 can be made or formed by fabric making techniques, such as braiding or twisting strands 104. For twisting, minimum number of strands 104 is two. For braiding, minimum number of strands 104 is three, as shown in FIG. 81. Braiding or intertwining three or more strands 104 provides excellent flexibility, strength and porosity of the filament 126. The snagging point 231 of cannula 230 and gripper 111 of needle 101 can catch, snag or engage the filament 126 well. The flexible filament 126 can also be woven, as shown in FIG. 82. Weaving is interlacing the strands 104 over and under each other, generally oriented at 90 degree angles. Half of the strands 104 from weaving can be oriented length-wise along the linear filament 126, to expedite capillarity or fluid flow from the muscle 193 or diffusion zones 106A, 106B into the degenerated disc 100. The flexible filament 126 can be knitted, as shown in FIG. 83. Knitting is a construction made by interlocking loops of one or more strands 104. A knitted filament 126 may have the greatest elastic expansion and compression capability, delivering the most fluid transport or exchange between disc 100 and body circulation during compression and relaxation of the disc 100. In addition, the knitted filament 126 in coils, spirals or reels may have the highest porosity to enhance fluid absorbency, creating a reservoir of nutrients/oxygen/pH buffer 131 for dispersing into various parts of the avascular disc 100, as shown in FIGS. 39-40. Furthermore, the coiled or spiraled filament 126 with knitted strands 104 provides an elastic cushion within the disc 100 to reduce loading and pain in the facet joints 129. The knitted filament 126 may be an excellent matrix or scaffolding for cell 277 attachment and proliferation. The knitted filament 126 may also provide highly expandable spirals for bulking sphincters to regain urinary or fecal control. The filament 126 can be made with non-woven strands 104. The term non-woven is used in fabric industry to include all other techniques, such as carded/needle-punched, spun bonded, melt blown or other. Combinations of fabric making techniques for the filament 126 can also be used with the needle 101 and cannula 230. The filament 126 is an oxygen/nutrient/pH buffer conduit 126 and a scaffold 126 for disc cell 277 and new disc matrix attachment.

Material and/or orientation of the filaments 126 can affect (1) flow rate, (2) tensile strength, (3) annular sealing, (4) porosity, (5) fluid absorbency, (6) snagging ability, (7) elasticity, (8) selectivity of solute transport, (9) scaffold attachment of cells, (10) flexibility, (11) durability, (12) sterilization technique, (13) fibrotic formation, (14) biocompatibility, and/or (15) bulking. A filament 126 is cut at a slanted angle, showing a cross-section of a filament 126; the strands 104 are slanted or diagonally oriented to the length-wise filament 126, as shown in FIG. 84. FIG. 85 shows cross-sections of strands 104 parallel to the filament 126, covered by a wrapper, sheath or cover 127. The parallel-oriented strands 104 and wrapper 127 can be manufactured by extrusion. The strands 104 can also be micro tubes, as shown in FIG. 86, parallel to the filament 126. A wrapper 127 is used to cover, retain, enclose or house the micro strands 104 to form a filament 126. An individual micro tubular strand 104 is capable of having capillary action, drawing nutrients/oxygen/pH buffer 131 through the filament 126 into the disc 100.

The strands 104 are preferred to be made with biocompatible and hydrophilic material, absorbing, retaining or drawing fluid with nutrients/oxygen/pH buffer solutes 131 from a tissue with low osmolarity to mid layer of the desiccated disc 100 with high osmolarity. The filament 126 can be a suture, approved for human implant. Instead of fastening tissue, the suture is used as the filament 126, transporting fluid from low to high osmolarity to alleviate back pain.

The filament 126 or fluid absorbing conduit 126 can be made with a hydrophilic sponge or foam with pores 124, as shown in FIG. 87, to transport and retain fluid in the disc 100. The pores 124 can be open, connecting to other pores 124. The pores 124 can also be closed, not connecting to other pores 124 to retain fluid and cells 277. The filament 126 can be solid, pore-less or dense, as shown in cross section in FIG. 88. The solid filament 126 is similar to a mono-filament suture 126. The mono-filament 126 is relatively stiff or contains a shape-memory to resist a spiral or coiled configuration. The spiraled mono-filament 126 elastically expands within tissue, which is suitable for elastic bulking of sphincters to treat urinary or fecal incontinence.

Disc degeneration is caused by a transport hindrance of interstitial fluid between the avascular disc 100 and body circulation, resulting in hypoxic and starvation conditions in the mid-layer of the disc 100. A fluid absorbing conduit 126 is implanted in the mid-layer of the disc 100 to draw and bridge between the superior 106A and inferior 106B diffusion zones of nutrients/oxygen/pH buffer 131 as shown in FIG. 89. Daily activity of patient generates 5,000-10,000 compression and relaxation pumping cycles per day. During the compression phase, the fluid absorbing conduit 126 disperses the nutrients/oxygen/pH buffer 131 to neutralize lactic acid 162 and nourish disc cells, as shown in FIG. 90. During the relaxation phase, the fluid absorbing conduit 126 absorbs or replenishes the fluid from body circulation in diffusion zones of endplates 105 containing the nutrients/oxygen/pH buffer 131, as shown in FIG. 91. The fluid absorbing conduit 126 in FIGS. 89-91 is implanted between 0 mm and 5 mm from the cartilaginous endplate 105 for drawing the fluid from body circulation containing nutrients/oxygen/pH buffer 131.

Shape resilience or elasticity is a preferred physical property of the fluid absorbing conduit 126 for maintaining contact with at least one diffusion zones 106 or between 0 mm and 5 mm from at least one endplates 105 to transport nutrients/oxygen/pH buffer 131 into the mid-layer of the disc 100 during multi-cycles of compression and relaxation. The solid lines in FIG. 90 shows the positions of the disc 100 and the fluid absorbing conduit 126 during compression phase of the disc 100, while the dash lines show the positions of the disc 100 and fluid absorbing conduit 126 during the relaxation phase. In FIG. 91, The solid lines shows the positions of the disc 100 and the fluid absorbing conduit 126 during relaxation phase of the disc 100, while the dash lines show the positions of the disc 100 and the fluid absorbing conduit 126 during the compression phase. The modulus of resilience can be calculated using the Young's modulus. The Young's elastic modulus of the fluid absorbing conduit 126 should be between 1 kPa and 20 GPa, or preferred between 50 kPa and 15 GPa for maintaining resiliency, position or location through cycles of compression and relaxation to draw from the diffusion zone 106A and/or 106B of nutrients/oxygen/pH buffer 131 from capillaries in endplate 105.

Disc cells 277 isolated from advanced degenerated human discs 100 are still capable of producing collagen and glycosaminoglycans in tissue culture with abundant supply of nutrients in proper pH. (Gruber H. E., Leslie K., Ingram J., Hoelscher G., Norton H. J., Hanley E. N. Jr.: Colony formation and matrix production by human anulus cells: modulation in three-dimensional culture, Spine, July 1, 29(13), E267-274, 2004. Johnstone B, Bayliss M T: The large proteoglycans of the human intervertebral disc, Changes in their biosynthesis and structure with age, topography, and pathology, Spine, March 15; 20(6):674-84, 1995.) Furthermore, stem cells have recently been found in degenerated discs. (Risbud M V, Gattapalli A, Tsai T T, Lee J Y, Danielson K G, Vaccaro A G, Albert T J, Garzit Z, Garzit D, Shapiro I: Evidence for skeletal progenitor cells in the degenerate human intervertebral disc, Spine, November 1; 32(23), 2537-2544, 2007.) Nutrient 131 deficiency and acidic pH may hinder disc 100 repair in-vivo.

The filament 126 or fluid absorbing conduit 126 is the nutrient/oxygen spigots and scaffolds for cell 277 survival and attachment, as shown in FIG. 42. With a continual or renewable supply of nutrients/oxygen/pH buffer 131, disc cells 277 resume making biosynthetic products 160, such as the water-retaining glycosaminoglycans and collagen, the major components of the nucleus 128 and annulus 378. In sheep study, newly formed glycosaminoglycans on nylon strands 104 of the filament 126 can be seen after 3 months using Safranin histological staining.

The rate of sulfate incorporation for biosynthesizing glycosaminoglycans is pH sensitive. The maximum rate of sulfate incorporation is under pH 7.2-6.9. The rate of sulfate incorporation drops about 32-40% in acidic pH within the disc [Ohshima H, Urban J P: The effect of lactate and pH on proteoglycan and protein synthesis rates in the intervertebral disc. Spine, September:17(9), 1079-82, 1992]. Hence, pH normalization with pH buffer 131 through the filament 126 will likely increase production of the water-retaining glycosaminoglycans and swelling pressure of the disc 100 packed with the fluid absorbing conduit 126.

With a continual supply of nutrients 131, newly formed biosynthetic products 160 increase osmolarity within the conduit-implanted disc 100, enhancing inward fluid flow, as shown in FIGS. 39, 40-42. The increased fluid flow comes through (1) the external filament 126, (2) blood capillaries 107 through the endplates 105, and/or (3) annulus 378. The fluid is also retained by the newly formed water-retaining glycosaminoglycans 160. As a result, the swelling pressure of the conduit-implanted disc 100 increases. Segmental or spinal instability is reduced. Muscle tension and ache from guarding the spinal instability decrease. Load and pain of the facet joints 129 decrease. Lactic acid 162 is further neutralized by inflow of nutrients/oxygen/pH buffering 131 to reduce or alleviate acid burn. Disc 100 height is elevated, raised or increased as depicted by arrows in FIGS. 40-41. Implantation of the fluid absorbing conduit 126 or filament 126 enables the degenerated disc 100 to be repaired.

Furthermore, adenosine triphosphate, ATP, is the high-energy compound essential for driving or energizing biochemical reactions, including the biosynthesis of the water retaining glycosaminoglycans for sustaining compressive loads on the disc 100. Under anaerobic conditions, metabolism of each glucose molecule produces only two ATP and two lactic acids 162, which irritate adjacent nerves 118. When oxygen 131 permeates through the internal and/or external conduit 126, thirty-six ATP can be produced from each glucose molecule through glycolysis, citric acid cycle and electron transport chain under aerobic conditions to energize disc regeneration and alleviate back pain.

High concentration of nutrients 131 can also be injected into the disc 100 implanted with the fluid absorbing conduit 126 to create high osmolarity instantly, as shown in FIGS. 43 and 46. High osmolarity promotes fluid inflow into the conduit-implanted disc 100. However, glucose or sugars injection can produce additional lactic acid 162, causing more pain. Sulfate and amino acids can be injected in high concentration to boost osmolarity and production of glycosaminoglycans and collagen, as the biosynthetic product 160 in FIG. 42. Magnesium sulfate, potassium sulfate, or sodium sulfate can be the injectable with high water solubility and are essential for biosynthesis of glycosaminoglycans in the nucleus pulposus 128. Proline and glycine can also be injectables with high water solubility and are essential nutrients 131 for biosynthesis of collagen in the annulus 378.

Anesthetic, anti-depressant, NSAID, antibiotics, anti-inflammatory steroid, alkaline agent, muscle relaxant, growth factor, calcium channel blocker, or other drugs can also be injected into the conduit-implanted disc 100 to instantaneously reduce pain, as shown in FIGS. 43 and 46.

Autograft disc cells 277 from a healthy disc 100 of the patient can be transplanted into the degenerated and conduit-implanted disc 100 to promote disc regeneration and production of biosynthetic product 160, as shown in FIGS. 43 and 46.

The avascular disc 100 is well sealed and immuno-isolated. Even small ions, such as sulfate, and small molecules, such as proline, are greatly limited from diffusing into the nucleus pulposus 128. The well sealed disc 100 may be able to encapsulate donor cells 277 from a disc 100 of another person, cadaver or even animal without triggering an immune response, and probably not needing anti-rejection drug. For disc 100 regeneration, the donor cells 277 can also be stem cells 277, notochord 277 or chondrocytes 277.

The molecular weights of nutrients/oxygen/pH buffer 131 and lactic acid 162 are much smaller than the immuno-responsive cells, i.e. giant cells, macrophages, mononuclear phagocyts, T-cells, B-cells, lymphocytes, Null cells, K cells, NK cells and/or mask cells. The transport selectivity can be regulated or limited by the size of the pores or channels within the semi-permeable fluid absorbing conduit 126. The upper molecular weight cut-off of the conduit 126 can be 100,000 or lower to allow the passage of nutrients and waste but exclude the immuno-responsive cells and cytokines. The semi-permeable conduit 126 may also contain ionic or affinity surfaces to attract nutrients/oxygen/pH buffer 131 and waste, including lactic acid 162. The surfaces of the semi-permeable conduit 126 can be made, coated or modified to repel, exclude or reject immuno-responsive components.

In recent years, cell transplants from cadavers or live donors have been successful in providing therapeutic benefits. For example, islet cells from a donor pancreas are injected into a type I diabetic patient's portal vein, leading into the liver. The islets begin to function as they normally do in the pancreas by producing insulin to regulate blood sugar. However, to keep the donor cells alive, the diabetic patient requires a lifetime supply of anti-rejection medication, such as cyclosporin A. In addition to the cost of anti-rejection medication, the side effects of these immuno-suppressive drugs may include cancer. The benefit of cell transplant may not out weigh the potential side effects.

The intervertebral disc 100 implanted with the conduit 126 can be used as a semi-permeable capsule to encapsulate the injected therapeutic donor cells 277, as shown in FIGS. 43, 46, to evade the immune response. Hence no life-long immuno-suppressive drug would be required. Donor cells 277 can be from the pituitary gland (anterior, intermediate lobe or posterior), hypothalamus, adrenal gland, adrenal medulla, fat cells, thyroid, parathyroid, pancreas, testes, ovary, pineal gland, adrenal cortex, liver, renal cortex, kidney, thalamus, parathyroid gland, ovary, corpus luteum, placenta, small intestine, skin cells, stem cells, gene therapy, tissue engineering, cell culture, other gland or tissue. The donor cells 277 are immunoisolated within the conduit-implanted discs 100, the largest avascular organs in the body, maintained by exchange of nutrients/oxygen/pH buffer 131 and waste through the fluid absorbing conduit 126. The donor cells 277 can be from human, animal or cell culture. When disc pressure is low during sleep or supine position, nutrients/oxygen/pH buffering solutes 131 are supplied through the fluid absorbing conduit 126 to the donor cells 277. During waking hours while the pressure within the disc 100 is high, biosynthesized products 160 by these donor cells 277 are expelled through the fissure 121 or endplate 105 into bodily circulation and target sites.

The biosynthesized product 160 made by the donor cells 277 can be adrenaline, adrenocorticotropic hormone, aldosterone, androgens, angiotensinogen (angiotensin I and II), antidiuretic hormone, atrial-natriuretic peptide, calcitonin, calciferol, cholecalciferol, calcitriol, cholecystokinin, corticotropin-releasing hormone, cortisol, dehydroepiandrosterone, dopamine, endorphin, enkephalin, ergocalciferol, erythropoietin, follicle stimulating hormone, γ-aminobutyrate, gastrin, ghrelin, glucagon, glucocorticoids, gonadotropin-releasing hormone, growth hormone-releasing hormone, human chorionic gonadotrophin, human growth hormone, insulin, insulin-like growth factor, leptin, lipotropin, luteinizing hormone, melanocyte-stimulating hormone, melatonin, mineralocorticoids, neuropeptide Y, neurotransmitter, noradrenaline, oestrogens, oxytocin, parathyroid hormone, peptide, pregnenolone, progesterone, prolactin, pro-opiomelanocortin, PYY-336, renin, secretin, somatostatin, testosterone, thrombopoietin, thyroid-stimulating hormone, thyrotropin-releasing hormone, thyroxine, triiodothyronine, trophic hormone, serotonin, vasopressin, or other therapeutic products. These biosynthetic products 160 have low molecular weights and are able to be transported through the endplate 105 and/or the fissures 121, while the donor cells 277 are trapped within the disc 100.

The biosynthesized products 160 (hormones, peptides, neurotransmitter, enzymes, catalysis or substrates) generated within the conduit-implanted disc 100 may be able to regulate bodily functions including blood pressure, energy, neuro-activity, metabolism, and activation and suppression of gland activities. Some hormones and enzymes govern, influence or control eating habits and utilization of fat or carbohydrates. These hormones or enzymes may provide weight loss or gain benefits. Producing neurotransmitters, such as dopamine, adrenaline, noradrenaline, serotonin or γ-aminobutyrate, from the donor cells 277 within the conduit-implanted disc 100 can treat depression, Parkinson's disease, learning disability, memory loss, attention deficit, behavioral problems, depression, mental or neuro-related diseases.

Release of the biosynthesized products 160 by the donor cells 277 within the conduit-implanted disc 100 is synchronized with body activity. During activities of daily living, the pressure within the conduit-implanted disc 100 is usually high to expel the biosynthesized products 160 by the donor cells 277 into circulation to meet the demands of the body. In the supine position, pressure within the conduit-implanted disc 100 is low; fluid inflow 161 through the fluid absorbing conduit 126 is favorable, bringing nutrients/oxygen/pH buffer 131 into the disc 100 to nourish the cells 277. As an example, islets of Langerhans from a donor's pancreas can be implanted or injected into the conduit-implanted disc 100. In supine position during sleeping, glucose enters into the conduit-implanted disc 100 to induce production of insulin from the implanted islets of Langerhans. During waking hours when disc pressure is high, insulin is expelled through the endplate 105 or fissure 121 into circulation to regulate concentration of glucose in the body. At night, the insulin released from the conduit-implanted disc 100 is minimal to prevent hypoglycemia. In essence, biosynthesized products 160 by the donor cells 277 are released concurrent with physical activity to meet the demands of the body.

Donor cells 277 can also be seeded on the fluid absorbing conduit 126 or injected days, weeks, months or even years after implanting the fluid absorbing conduit 126 as shown in FIG. 43 to ensure favorable biological conditions, including pH, electrolytic balance and nutrients/oxygen/pH buffer 131, for cell 277 survival and proliferation in the conduit-implanted disc 100.

In the United States, average age of patients undergoing back surgery is about 40-45 years old. The fluid absorbing conduit 126 is preferred to be made with permanent material to provide long-lasting pain relief. A wide range of non-degradable materials can be used to fabricate the fluid absorbing conduit 126. Polymers, such as nylon, polytetrafluoroethylene, polypropylene, polyethylene, polyamide, polyester, polyurethane, silicon, poly-ether-ether-ketone, acetal resin, polysulfone, polycarbonate, silk, cotton, or linen are possible candidates. The fluid absorbing conduit 126 can also be made with collagen, proteoglycans, hyaluronate or other biomaterials.

Especially for investigative purposes, biodegradable fluid absorbing conduit 126 may provide evidence of efficacy within weeks or months. Since the fluid absorbing conduit 126 degrades within months, any unforeseen adverse outcome would be dissipated. If the investigative-degradable fluid absorbing conduit 126 shows promise, permanent fluid absorbing conduit 126 can then be implanted to provide continuous benefits. The biodegradable fluid absorbing conduit 126 can be made with polylactate, polyglycolic, poly-lactide-co-glycolide, polycaprolactone, trimethylene carbonate, silk, catgut, collagen, poly-p-dioxanone or combinations of these materials. Other degradable polymers, such as polydioxanone, polyanhydride, trimethylene carbonate, poly-beta-hydroxybutyrate, polyhydroxyvalerate, poly-gama-ethyl-glutamate, poly-DTH-iminocarbonate, poly-bisphenol-A-iminocarbonate, poly-ortho-ester, polycyanoacrylate or polyphosphazene can also be used.

The fluid absorbing conduit needle 101 and cannula 230 can be made with stainless steel, nickel-titanium alloy, or other alloy. The fluid absorbing conduit needle 101 and cannula 230 can also be made with polymers through extrusion and/or mold injection. The needle 101 and cannula 230 can be coated with lubricant, tissue sealant, analgesic, antibiotic, radiopaque, magnetic and/or echogenic agents.

Discitis is a painful infection or inflammatory lesion in the intervertebral disc 100 of adults and children (Wenger D R, Bobechko W P, Gilday D L: The spectrum of intervertebral disc-space infection in children, J. Bone Joint Surg. Am., 60:100-108, 1978. Shibayama M, Nagahara M, Kawase G, Fujiwara K, Kawaguchi Y, Mizutani J: New Needle Biopsy Technique for Lumbar Pyogenic Spondylodiscitis, Spine, 1 November, Vol. 35—Issue 23, E1347-E1349, 2010). Due to the avascular nature of the disc 100, oral or intravenous drugs cannot easily reach the bacteria or inflammation within the disc 100. Therefore, discitis is generally difficult to treat. The fluid absorbing conduit 126 can draw the oral antibiotics, anti-inflammatory drugs, anesthetics or other drugs from diffusion zone 106A or 106B deep into the avascular disc 100 to treat infection, inflammation, pain, tumor or other disease.

Staphylococcus aureus is the most common bacteria found in discitis. The fluid absorbing conduit 126 can be loaded or coated with an antibiotic, such as nafcillin, cefazolin, dicloxacilin, clindamycin, bactrim, penicillin, amoxicillin, mupirocin (bactroban), vancomycin, linezolid, rifampin, sulfamethoxazole-trimethoprim or other, to treat staphylococcus aureus infection. Corynebacterium is also found in discitis. The fluid absorbing conduit 126 can be loaded or coated with an antibiotic, such as erythromycin, vancomycin, eifampin, penicillin or tetracycline, to treat corynebacterium infection. Other antibiotics, such as cefdinir, metronidazole, tinidazole, cephamandole, latamoxef, cefoperazone, cefmenoxime, furazolidone or other, can also be used to coat the fluid absorbing conduit 126. The antibiotics 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

Inflammation in the disc 100 can cause excruciating pain. MRI can show inflammation at the endplates 105, and distinguish inflammatory classification as Modic I, II or III. The fluid absorbing conduit 126 can be coated or loaded with nonsteroidal anti-inflammatory drugs/analgesics (NSAID), such as aspirin, diflunisal, salsalate, ibuprofen, naproxen, fenoprofen, ketoprofen, flurbiprofen, oxaprozin, indomethacin, sulindac, etodolac, ketorolac, diclofenac, nabumetone, piroxicam, meloxicam, tenoxicam, droxicam, lornoxicam, isoxicam, mefenamic acid, meclofenamic acid, flufenamic acid, tolfenamic acid, celecoxib, rofecoxib, valdecoxib, parecoxib, lumiracoxib, etoricoxib, firocoxib, nimesulide, licofelone or other NSAID, to treat inflammation in the disc 100 for pain relief. The NSAID 131can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can also be coated or loaded with steroidal anti-inflammatory drugs/analgesics, such as betamethasone, budesonide, cortisone, dexamethasone, hydrocortisone, methylprednisolone, prednisolone, prednisone, triamcinolone or other steroid, to treat inflammation in the disc 100 for pain relief. The steroidal anti-inflammatory drug 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with anesthetics, such as procaine, amethocaine, cocaine, lidocaine, prilocaine, bupivacaine, levobupivacaine, ropivacaine, mepivacaine, dibucaine, methohexital, thiopental, diazepam, lorazepam, midazolam, etomidate, ketamine, propofol, alfentanil, fentanyl, remifentanil, sufentanil, buprenorphine, butorphanol, diamorphine, hydromorphone, levophanol, meperidine, methadone, morphine, nalbuphine, oxycodone, oxymorphone, pentazocine or other anesthetic, to provide instant pain relief. The anesthetic 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with a muscle relaxant, such as succinylcholine, decamethonium, mivacurium, rapacuronium, atracurium, cisatracurium, rocuronium, vecuronium, alcuronium, doxacurium, gallamine, metocurine, pancuronium, pipecuronium, tubocurarine or other relaxant, to relieve muscle tension and ache. The muscle relaxant 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with buffering agents, such as sodium carbonate, sodium bicarbonate, potassium carbonate, potassium bicarbonate, magnesium carbonate, calcium carbonate, barium carbonate, potassium phosphate, sodium phosphate or other buffering agent, to neutralize lactic acid 162 and spontaneously alleviate pain caused by acid irritation or burn. The buffering agent 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with alkaline agents, such as magnesium oxide, magnesium hydroxide, sodium hydroxide, potassium hydroxide, barium hydroxide, cesium hydroxide, strontium hydroxide, calcium hydroxide, lithium hydroxide, rubidium hydroxide, neutral amines or other alkaline agent, to neutralize lactic acid 162 and spontaneously alleviate pain caused by acid irritation. The alkaline agent 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with initial supplies of nutrients 131, such as sulfate, glucose, glucuronic acid, galactose, galactosamine, glucosamine, hydroxylysine, hydroxylproline, serine, threonine, chondroitin sulfate, keratan sulfate, hyaluronate, magnesium trisilicate, magnesium mesotrisilicate, magnesium oxide, magnosil, orthosilicic acid, magnesium trisilicate pentahydrate, sodium metasilicate, silanolates, silanol group, sialic acid, silicic acid, boron, boric acid, other mineral, other amino acid or nutrients 131, to enhance or initiate production of sulfated glycosaminoglycans and collagen within the degenerative disc 100. The nutrients 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with growth factor 131. Bone morphogenic protein (BMP) is a growth factor, known to accelerate production of proteoglycans in thin (1-3 mm) animal discs, where diffusion depth of nutrient and oxygen is sufficient. Platelet rich plasma (PRP) contains several growth factors, i.e. transforming growth factor beta-1 (TGFB1), platelet-derived growth factor (PDGF), insulin-like growth factor 1, and vascular endothelial growth Factor. Transforming growth factor beta-1 was shown to stimulate production of proteoglycans and collagen in ex-vivo and in thin animal discs. The growth factor 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

Oral intake of antidepressants has shown temporary pain reduction or pain tolerance in back pain patients. Anti-depressants can be coated on the fluid absorbing conduit 126 to treat chronic back pain. The anti-depressant coating may include tricyclic antidepressant, serotonin-reuptake inhibitor, norepinephrine reuptake inhibitor, serotonin-norepinephrine reuptake inhibitor, noradrenergic/serotonergic antidepressants, norepinephrine-dopamine reuptake inhibitor, serotonin reuptake enhancers, norepinephrine-dopamine disinhibitors or monoamine oxidase inhibitor. The antidepressant can be amitriptyline, amitriptylinoxide, butriptyline, clomipramine, demexiptiline, desipramine, dibenzepin, dimetacrine, dosulepin/dothiepin, doxepin, duloxetine, imipramine, imipraminoxide, lofepramine, melitracen, metapramine, nitroxazepine, nortriptyline, noxiptiline, pipofezine, propizepine, protriptyline, quinupramine, amineptine, iprindole, opipramol, tianeptine, trimipramine, or other antidepressant. The antidepressant 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

Fibrous formation over the fluid absorbing conduit 126 may affect the exchange of nutrients/oxygen/pH buffer 131 and waste between the disc 100 and bodily circulation or muscle 193. Immuno inhibitor can be coated or incorporated into the fluid absorbing conduit 126 to minimize fibrous formation or tissue response. Examples of immuno inhibitors include but are not limited to: actinomycin-D, aminopterin, azathioprine, chlorambucil, corticosteroids, crosslinked polyethylene glycol, cyclophosphamide, cyclosporin A, 6-mercaptopurine, methylprednisolone, methotrexate, niridazole, oxisuran, paclitaxel, polyethylene glycol, prednisolone, prednisone, procarbazine, prostaglandin, prostaglandin E₁, sirolimus, steroids or other immune suppressant drugs. The immuno inhibitor 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with a calcium channel blocker for inhibiting activation of neuro-receptor to alleviate pain. The calcium channel blocker can be dihydropyridines, phenylalkylamines, benzothiazepines, magnesium ion, Amlodipine, Felodipine, Isradipine, Lacidipine, Lercanidipine, Nicardipine, Nifedipine, Nimodipine, Nisoldipine, Verapamil, Diltiazem or other calcium channel blocker. The calcium channel blocker 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

Healthy intervertebral discs 100 are avascular. To ensure avascular conditions, the fluid absorbing conduit 126 can be incorporated, coated or partially coated with an anti-angiogenic compound. Examples of anti-angiogenic compounds include, but are not limited to, Marimastat from British Biotech [a synthetic inhibitor of matrix metalloproteinases (MMPs)], Bay 12-9566 from Bayer (a synthetic inhibitor of tumor growth), AG3340 from Agouron (a synthetic MMP inhibitor), CGS 27023A from Novartis (a synthetic MMP inhibitor), COL-3 from Collagenex (a synthetic MMP inhibitor, Tetracycline® derivative), Neovastat from Aeterna, Sainte-Foy (a naturally occurring MMP inhibitor), BMS-275291 from Bristol-Myers Squib (a synthetic MMP inhibitor), TNP-470 from TAP Pharmaceuticals, (a synthetic analogue of fumagillin; inhibits endothelial cell growth), Thalidomide from Celgene (targets VEGF, bFGF), Squalamine from Magainin Pharmaceuticals (Extract from dogfish shark liver; inhibits sodium-hydrogen exchanger, NHE3), Combretastatin A-4 (CA4P) from Oxigene, (induction of apoptosis in proliferating endothelial cells), Endostatin collagen XVIII fragment from EntreMed (an inhibition of endothelial cells), Anti-VEGF Antibody from Genentech, [Monoclonal antibody to vascular endothelial growth factor (VEGF)], SU5416 from Sugen (blocks VEGF receptor signaling), SU6668 from Sugen (blocks VEGF, FGF, and EGF receptor signaling), PTK787/ZK 22584 from Novartis (blocks VEGF receptor signaling), Interferon-alpha (inhibition of bFGF and VEGF production), Interferon-alpha (inhibition of bFGF and VEGF production), EMD121974 from Merck, KcgaA (small molecule blocker of integrin present on endothelial cell surface), CAI from NCI (inhibitor of calcium influx), Interleukin-12 from Genetics Institute (Up-regulation of interferon gamma and IP-10), IM862 from Cytran, Avastin, Celebrex, Erbitux, Herceptin, Iressa, Taxol, Velcade, TNP-470, CM101, Carboxyamido-triazole, Anti-neoplastic urinary protein, Isotretionin, Interferon-alpha, Tamoxifen, Tecogalan combrestatin, Squalamine, Cyclophosphamide, Angiostatin, Platelet factor-4, Anginex, Eponemycin, Epoxomicin, Epoxy-β-aminoketone, Antiangiogenic antithrombin III, Canstatin, Cartilage-derived inhibitor, CD59 complement fragment, Fibronectin fragment, Gro-beta, Heparinases, heparin hexasaccharide fragment, Human chorinonic gonadotropin, Interferon (alpha, beta or gamma), Interferon inducible protein (IP-10), Interleukin-12 (IL-12), Kringle 5 (plasminogen fragment), Tissue inhibitors of metalloproteinases, 2-Methoxyestradiol (Panzem), Placental ribonuclease inhibitor, Plasminogen activator inhibitor, Prolactin 16 kD fragment, Retinoids, Tetrahydrocortisol-S, Thrombospondin-1, Transforming growth factor beta, Vasculostatin, and Vasostatin (calreticulin fragment). The anti-angiogenic compound 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

The fluid absorbing conduit 126 can be loaded or coated with lactic acid inhibitor or lactate dehydrogenase inhibitor. The lactic acid inhibitor or lactate dehydrogenase inhibitor includes fluoropyruvic acid, fluoropyruvate, levulinic acid, levulinate, oxamic acid, N-substituted oxamic acids, oxamate, oxalic acid, oxalate, beta-bromopropionate, beta-chloropropionate, malonate, sodium formaldehyde bisufite, chloroacetic acid, alpha-chloropropionate, alpha-bromopropionate, beta-iodopropionate, acrylate, acetoin, malic acid, glycolate, diglycolate, acetamide, acetaldehyde, acetylmercaptoacetic acid, alpha ketobutyrate, thioglycolic acid, nicotinic acid, alpha-ketoglutarate, butanedione, hydroxypyruvic, chloropyruvic, bromopyruvic, 2,3-dihydroxy-6-methyl-4-(1-methylethyl)-1-naphthoic acid, diethyl pyrocarbonate, hexyl N,N-diethyloxamate, 3-acetylpyridine adenine dinucleotide, 7-p-Trifluoromethylbenzyl-8-deoxyhemigossylic acid, dihydroxynaphthoic acids, N-substituted oxamic acids, gossypol, gossylic iminolactone, derivatives of gossypol, dihydroxynaphthoic acid, 2, 3-dihydroxy-6-methyl-4-(1-methylethyl)-1-naphthoic acid, blue dye, reactive blue dye #2 (Cibacron Blue 3G-A) urea, methylurea and hydantoic acid, glyoxylate, hydroxybutyrate, 4-hydroxyquinoline-2-3carboxylic acids, sodium bisulfite, dieldrin, L-(+) beta monofluorolactic acid, fluoro-lactic acid, tartronic acid, mesotartarate, sesquiterpene 8-deoxyhemigossylic acid (2, 3-dihydroxy-6-methyl-4-(1-methylethyl)-1-naphthoic acid), or analogues of these chemicals. The lactic acid inhibitor or lactate dehydrogenase inhibitor 131 can also be injected into the conduit-implanted disc 126, as shown in FIG. 43 or 46.

In summary, the fluid absorbing conduit 126 alleviates back pain and/or regenerates the disc 100 by (1) drawing nutrients/oxygen/pH buffer 131 into the disc 100, (2) neutralizing lactic acid 162 to alleviate acid burn, (3) converting anaerobic to aerobic conditions to reduce lactic acid 162 production, (4) increasing sulfate incorporation in neutral pH for biosynthesis of glycosaminoglycans. (5) increasing ATP production from aerobic metabolism of sugars to drive biosynthetic reactions in disc 100, (6) bulking up the disc 100 to take load off painful facet joints 129, (7) fortifying the disc 100 to reduce spinal instability and muscle tension, (8) rebuilding disc matrix to increase osmolarity, fluid intake and absorption, (9) re-establishing the swelling pressure to sustain disc 100 compression, (10) regenerating the disc 100 for long term pain relief, (11) delivering systemic drugs in disc 100 to treat discitis, and/or (12) working with therapeutic agents 131 to expedite pain relief and/or disc 100 regeneration.

Unlike many surgical interventions of the spine, benefits of the fluid absorbing conduit 126 include (1) spinal motion preservation, (2) no tissue removal, (3) reversible by extraction, (4) micro-invasive, (5) out-patient procedure, (6) approved implant material, (7) 15-30 minutes per disc, (8) long-lasting and no-harm-done, (9) no incision, (10) compatible with drugs, conservative treatment or surgical intervention, if needed, and (11) drug coated fluid absorbing conduit 126 if needed to expedite pain relief.

The fluid absorbing conduit 126 or filament 126 is implanted in the intervertebral disc 100 between 0 mm and 5 mm from at least one endplate 105 to draw fluid from body circulation containing nutrients/oxygen/pH buffer 131 from capillaries 107 at the endplate 105, as depicted in FIGS. 40, 89-91. The nutrients/oxygen/pH buffer 131 is delivered through the fluid absorbing conduit 126 into the mid layer of the disc 100. The intervertebral disc 100 undergoes thousands of compression and relaxation cycles per day. The fluid absorbing conduit 126 should be elastic, resilient or malleable to remain in position or location between 0 mm and 5 mm from at least one endplate 105 to draw the nutrients/oxygen/pH buffer 131 from the body circulation. The fluid absorbing conduit 126 can be a filament, sponge, gel, hydrogel, polymer, biomaterial or other material having resiliency with Young's elastic modulus between 1 kPa and 20 GPa, or preferred modulus between 50 kPa and 15 GPa for maintaining position or location between 0 mm and 5 mm from at least one endplate 105. Therapeutic agent 131 can also be coated on the fluid absorbing conduit 126 or injected into the conduit-implanted disc 100 to expedite pain relief and disc 100 regeneration.

The implant procedure of the fluid absorbing conduit 126 does not enter bone. Spine surgeon, orthopedic surgeon, pain interventionist, interventional radiologist, anesthesiologist, or neurosurgeon is qualified to implant the fluid absorbing conduit 126, or to inject therapeutic agent 131 into conduit-implanted disc 100.

It is to be understood that the present invention is by no means limited to the particular constructions disclosed herein and/or shown in the drawings, but also includes any other modification, changes or equivalents within the scope of the claims. Many features have been listed with particular configurations, curvatures, options, and embodiments. Any one or more of the features described may be added to or combined with any of the other embodiments or other standard devices to create alternate combinations and embodiments. A pH electrode may be exposed near the tip of the needle 101 to detect the acidity within the disc 100.

It should be clear to one skilled in the art that the current embodiments, materials, constructions, methods, tissues or incision sites are not the only uses for which the invention may be used. The fluid absorbing conduit 126 can be a filament 126, strand 126, thread 126, shunt 126, wick 126, sponge 126, gel 126 or absorbent 126. Spiraled filament 126 can be called a spiraled conduit 126, coiled filament 126 or coiled shunt 126. The snagging point 231 can be called the snagger 231. The filament gripper 111 can be called the gripper 111. Nothing in the preceding description should be taken to limit the scope of the present invention. The full scope of the invention is to be determined by the appended claims. 

What is claimed is:
 1. A method for relieving pain and/or regenerating an intervertebral disc, the method comprising the steps of: (a) inserting a fluid absorbing conduit sized and configured into the intervertebral disc, between 0 mm and 5 mm from at least one of the endplates; (b) drawing fluid from body circulation from the at least one endplate into said fluid absorbing conduit, wherein the fluid from body circulation comprises bicarbonate, oxygen and nutrients; (c) and transporting the bicarbonate, oxygen and nutrients from said fluid absorbing conduit into a mid-layer of the intervertebral disc, thereby neutralizing the lactic acid in the mid-layer by the bicarbonate to relieve discogenic pain, and thereby nourishing disc cells with oxygen and nutrients to regenerate the intervertebral disc.
 2. The method of claim 1, further comprising the step of: (d) injecting a therapeutic agent into the intervertebral disc.
 3. The method of claim 1, further comprising the step of: (d) puncturing the intervertebral disc with a needle comprising a syringe, wherein said syringe comprises a therapeutic agent; (e) and injecting said therapeutic agent through said syringe and needle into the intervertebral disc.
 4. The method of claim 1, further comprising the step of: (d) inserting a cannula into the intervertebral disc, wherein said fluid absorbing conduit in the step (a) is inserted through said cannula.
 5. The method of claim 4, further comprising the step of: (e) injecting a therapeutic agent into the intervertebral disc through said cannula.
 6. The method of claim 1, wherein said fluid absorbing conduit has water absorbency between 10% and 500% of said fluid absorbing conduit weight after water saturation.
 7. The method of claim 1, wherein said fluid absorbing conduit has water contact angle between 0 and 60 degrees.
 8. The method of claim 1, wherein said fluid absorbing conduit is a resilient or malleable sponge.
 9. The method of claim 1, wherein said fluid absorbing conduit is a gel.
 10. The method of claim 1, wherein said fluid absorbing conduit is a polymeric material.
 11. The method of claim 1, wherein said fluid absorbing conduit is collagen.
 12. The method of claim 1, wherein said fluid absorbing conduit is proteoglycans.
 13. The method of claim 1, wherein said fluid absorbing conduit is hyaluronate.
 14. The method of claim 2, wherein said therapeutic agent is a pH buffering agent.
 15. The method of claim 2, wherein said therapeutic agent is an antibiotic.
 16. The method of claim 2, wherein said therapeutic agent is an anti-inflammatory drug.
 17. The method of claim 2, wherein said therapeutic agent is an anesthetic.
 18. The method of claim 2, wherein said therapeutic agent is an antacid or alkaline agent.
 19. The method of claim 2, wherein said therapeutic agent is a nutrient and/or sulfate.
 20. The method of claim 2, wherein said therapeutic agent is an anti-depressant.
 21. The method of claim 2, wherein said therapeutic agent is a calcium channel blocker.
 22. The method of claim 2, wherein said therapeutic agent is a growth factor.
 23. The method of claim 2, wherein said therapeutic agents are cells. 